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This on-demand teaching session will give medical professionals background knowledge on introduction to arthritis and the related diseases, including CPPD crystal deposition disease, Scleroderma, and Systemic Lupus Erythematosus. The lecture will cover the radiographic findings, key findings, and common presentations of each disease. Medical professionals can expect to learn about the characteristic distributions of each disorder to assist in making a correct diagnosis. The course also provides an opportunity to discuss and ask questions in the comments section, as well as receiving notifications of future lectures.
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This is the third in a series of lectures about diagnostic techniques used to differentiate the arthritides using a target area approach radiographically.

In part two of the series, we discussed juvenile rheumatoid arthritis, erosive osteoarthritis, septic arthritis, and the seronegative spondyloarthropathies.

In part three, we will continue discussing further arthritis topics such as CPPD crystal deposition disease, scleroderma, SLE, sarcoid, neuropathic arthropathy, hemophilia, CRMO, and SAPHO syndrome.

Learning objectives

Learning Objectives: 1. Describe the key findings of calcium pyrophosphate dihydrate crystal deposition disease. 2. Identify the radiographic findings of scleroderma and explain the pathophysiology of calcifications. 3. Identify the common distribution of SL E in the hands and list relevant extra findings. 4. Explain how the characteristic deformities in SL E are different in a raised and lowered hand. 5. Compare and contrast the clinical presentations of calcium pyrophosphate dihydrate crystal deposition disease, scleroderma, and systemic lupus erythematosus.
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Computer generated transcript

The following transcript was generated automatically from the content and has not been checked or corrected manually.

We're live now Dennis. OK. Just a moment that n good morning or good afternoon. However, you feel about today and the daylight saving time, it's really nice that you all have joined us for these lectures. Remember that the first two lectures are available on this platform for on-demand viewing. And I urge you to do so because the note you can take notes on on demand and you can learn the subject really well. This is the last lecture of this series, but I will generate more lectures as time passes and provide them for you. You will receive notifications from me by email. Finally, please fill out the evaluation form that is located on this platform. It gives me insights into my lecture techniques and also what topics you would like to have covered. Add these to the comments, please. And remember however, that advanced imaging is beyond the scope of this training exercise. I want to give you background in general M SK radiology, but also can cover interpretation of chest and abdomen. More knowledge and understanding will make you a more efficient and more accurate film viewer. Today, we will cover the final group of the diseases in this lecture about introduction to arthritis. So let's begin. We will, we will begin today's lecture by discussing calcium pyrophosphate dihydrate crystal deposition disease. My favorite disease, the key findings in this disorder are chondrocalcinosis located at the triangular fibrocartilage complex of the wrist or in the meniscal tissue in the knee or in the symphysis pubis calcium pyrophosphate dihydrate crystal deposition disease is a long name for an inflammatory joint disease caused by deposition of this crystal in the synovial fluid synovial lining and articular cartilage. This disorder is the second most common degenerative disease seen in man following osteoarthrosis. It causes characteristic degenerative changes in very specific locations. There are several terms that you need to be familiar with when talking about CPPD crystal deposition disease. Chondrocalcinosis is a descriptive term describing fine fine calcifications in cartilage most often used when CPPD crystal is the cause. However, chondrocalcinosis is not an exclusive feature of CPPD crystal deposition disease and can also be seen in severe osteoarthritis when it is seen in severe osteoarthritis. It is a combination disorder in was which both entities exist together. Pyrophosphate. Arthropathy is a distinctive arthropathy of CPPD crystal deposition disease which is like osteoarthritis but has an unusual and very specific distribution. Pseudogout is an acute joint inflammation secondary to C PBD crystals. It is called pseudogout because clinically it can look like gout. The radiographic findings of this disorder using our ABCD ES mnemonic A as before are no erosions are present in the articular surfaces. The bones demonstrate subchondral cyst formation which is exceedingly common. The cartilage demonstrates joint space narrowing. The distribution is symmetric, affecting the radiocarpal joint not shown here. The carpometacarpal joints and the metacarpophalangeal joints of the index and long fingers. C PBD arthropathy can also affect the elbow, the hip, the symphysis pubis, the knee and the ankle. There are no extra findings in this disorder. The soft tissue findings as we have discussed are chondrocalcinosis which when found in hyaline cartilage is linear as seen in the hip. But when found in the triangular fibrocartilage, it may occur in patchy fine distribution. Let us look at some patients with this disorder. Here are two different patients demonstrating classic findings of CPPD crystal deposition disease. In the left radiograph, we see cartilage loss in many joints and chondrocalcinosis in the carpal metacarpal joints of the base of the thumb indicated by the whi white arrow. The metacarpophalangeal joints of the index finger indicated by the arrowhead and the triangular fibrocartilage complex indicated by the asterisk. It is also important to note the radiocarpal joint space degenerative changes, particularly that on the scaphoid side. This is characteristic place for joint space narrowing in this disorder. In the right radiograph, we see chondrocalcinosis in the radiocarpal joint and the triangular fibrocartilage complex indicated by the black arrows. Scapholunate dissociation is also seen which is a common late finding in this disorder. However, scapholunate dissociation may also be seen in rheumatoid arthritis or po posttrauma. Here we see two different ap radiographs of the knee calcification in the cartilage and menisci are noted bilaterally on the right side indicated by the white arrow as well as on the left side indicated by the black arrow. Many times. This calcification is rather linear or clumped as we see here, which is also characteristic for CPPD crystal deposition disease. These calcifications can be caused by other conditions such as gout, but this is rarely rarely seen. In this case. Also note the joint space narrowing and mild osteophyte formation. Cppd crystal deposition disease has many features like osteoarthrosis. However, its distribution is completely different in these radiographs. The right image is a magnification of the left image we see well circumcised, well circumscribed coarse calcification adjacent to the fourth digital interphalangeal joint. This does not look like CPPD crystal deposition disease and scleroderma would be the more likely condition. However, aspiration revealed typical CPPD crystal depositions from this region. As in other arthropathies. Atypical presentations of CPPD crystal are possible but fortunately are less common in the future. I will do a lecture for you completely covering CPPD crystal deposition disease as well as hydroxy appetite crystal deposition disease and gout and the differences radiographically between the three diseases. Please learn the pattern of distribution which consists of moderate to severe degenerative changes at the radiocarpal joint, multiple subchondral cysts in the wrists of usually multiple sizes also changes at the metacarpophalangeal joints of the index and long fingers consisting of metacarpal head enlargement and beak formation on the thumb side of the metacarpals. I will show you examples of these. This distribution is only seen in two diseases. CPPD crystal deposition disease demonstrates this pathology at the index and long finger, metacarpophalangeal joints. While the disease hemochromatosis affects all four digits. Here we see two radiographic images of the hand and wrist taken from radio pia. The beaklike osteophytes are noted in both images at the metacarpal heads of the index and long fingers. Also findings compatible with CPPD include base of the thumb, degenerative changes, mild degenerative changes of the radiocarpal joint and scapholunate dissociation. Chondrocalcinosis is not present in this case and does not have to be present to diagnose C PBT changes. We will talk about this disease more in detail in the next lecture. Now we move on to a group of different diseases that have bone and joint involvement. The first disease that were going to talk about is scleroderma, scleroderma, also known as systemic sclerosis is an autoimmune connective tissue disease that is characterized by microvascular obliteration and sclerosis of the skin and internal organs. The key radiographic findings are soft tissue calcification and acroosteolysis which is absorption of the distal Tufts of the terminal Phala phalanges. The clinical harm hallmark of this disease is the appearance of taut tethering of the skin. The skin becomes very shiny and loses its characteristic lines and marks clinically even arthritis occurs in up to 65% of patients. And this may be one of the earliest manifestations of scleroderma. There is also a limited and multisystem variant of this disease. The crest syndrome is a common type of limited scleroderma consisting of skin calcinosis, Raynaud phenomena, esophageal dysmotility, sclerodactyly and tele ectasia. The systemic variant can affect virtually every organ system or can it can be localized. The radiographic findings include articular changes that involve the presence of erosions, pencil and cup deformity, resorption of the first carpal metacarpal joint with radial subluxation in the bones. We see acroosteolysis which is resorption of the terminal Tufts of the distal phalanges and periarticular osteopenia. The cartilage is affected in scleroderma demonstrating joint space narrowing. The distribution of the disease is noted in the, in illustration to the right involving the distal phalanges of the first index, long and ring fingers. The fifth finger is rarely affected. There is no foot involvement in scleroderma in the skeleton, scleroderma may affect the elbow, distal ulna, ischial tuberosities and the tibiotalar joint as extra findings. Scleroderma has multiple other organ manifestations including pulmonary and abdominal organ af affectation. The soft tissues are thickened, cutaneous calcifications are often seen particularly at medi mechanically exposed locations and at the acro soft tissue causing necrosis which you will see at the fingertips, soft tissue calcification. In scleroderma are often extensive in the distal phalanges. Here we see an example of this notice, the calcifications next to the distal ulna demonstrated by the arrow, there are no signs of cartilage damage. In this case, the pathophysiology of the calcium deposits is not well understood. It occurs in soft tissues that are under chronic stress such as local trauma or damage associated with an underlying inflammatory process. It is usually more abundant in the dominant hand. When these findings are present, the diagnosis is usually straightforward. Here, in another patient with scleroderma, we see subtle but coarse calc soft tissue calcifications at the most distal part of the index finger, no acroosteolysis or other signs are present. Severe acroosteolysis of the fingertips is noted in this patient at the distal aspects of the thumb, index finger and long fingers. Notice the lysis of the soft tissue distally. Acroosteolysis is the radiographic finding that refers to bone destruction of the distal phalanges and occurs in 6 to 65% of patients with scleroderma vascular alterations and reduced capillary density impair tissue oxygenation. And the resulting hypoxia may contribute to osteoclast activation. There is a wide variety of diseases that can cause acroosteolysis, including psoriatic arthritis infections, Raynaud's disease and thermal trauma. The image labeled A we see subcutaneous and periarticular calcifications in the foot of a patient with scleroderma. There is also a hallux valgus deformity which is not caused by scleroderma. In the image labeled b, subcutaneous calcifications near the elbow are noted in a patient with scleroderma. These subcutaneous calcifications often form at pressure points. Now we move, we will move on to another systemic disease that demonstrates articular findings, systemic lupus erythematosus. The key findings in SL E are abnormal joint alignment without erosions and with a vascular necrosis. Clinically, SL E is a generalized autoimmune connective tissue disease. Essentially, any organ system can be affected with systemic findings including muscle weakness, malaise and fever, mucocutaneous findings demonstrated by a typical butterfly rash on the face and renal and neurologic symptoms. The radiographic findings are that in the diagram, sl E affects the base of the tongue and the proximal and distal interphalangeal joints. It also affects the metacarpophalangeal joints and the proximal interphalangeal joints of the remaining fingers. It does not affect the foot involvement in the general skeleton includes the shoulder, the hip and the ankle joint. No erosions are noted. Periarticular osteoporosis or osteopenia occurs the cartilage in the joint. In a patient with scleroderma demonstrates normal joint spaces. The distribution in the hand is as seen in the diagram. It affects the base of the thumb, all metacarpophalangeal joints and all proximal interphalangeal joints. The distal interphalangeal joints are not affected. The extra findings in this disease include avascular necrosis. A specific and unusual finding in scleroderma in the soft tissues consists of reducible deformities like swan neck and boutonniere deformities. When the patient raises their hand, these deformities are clearly seen. However, when that hand is placed flat on a table, the deformities spontaneously reduce soft tissue swelling and calcifications in the subcutaneous and deep soft tissues may be also seen most often around small joints. Here in a patient with SL E, we see two ap views of the hands, Z like thumb deformities and swan neck fingers. The deformities are thought to be a consequence of low grade inflammation of the synovial membrane and capsule resulting in ligamentous laxity and muscular contraction. Here in another patient with systemic lupus erythematosus, we see another example of swan neck deformities, no erosions or signs of cartilage damage are noted. And yet another patient with scleroderma. Here we see swan neck deformities. As I mentioned earlier, these changes are usually reversible in the early stages of the disease. If this patient were to pledge their hand on the table top the fingers and the joints would take their normal position. Avascular necrosis is a frequent complication in SL E seen in up to 15% of patients. The femoral head and tibial plateau are the most involved sites but other sites may be affected as well. These patients have bone pa. If these patients have bone pain, one should be suspicious of having a vascular necrosis. A vascular necrosis in SL E can occur even in the absence of steroid use. Here, we see subtle increased density in the distal femur in a ser somewhat serpentine pattern, re re representing a vascular necrosis. In a patient with SL E moving on. We see radiographs of two different joints. In the lim image labeled A, we see subluxation of the first metacarpophalangeal joint without erosions in a patient with SL E. This is not typical for SL E and can be seen in other forms of as arthritis as well. In image B, we see SL E of the shoulder. This is demonstrated by collapse of the humeral head with some loose bony fragments lead to avascular necrosis, both steroid therapy and SL E are associated with increased risks of avascular necrosis. Now we move on to our next disease, which is a multisystem disorder of unknown etiology characterized by the formation of inflammatory noncaseating granulomas. This is sarcoid. The key findings in sarcoid are lacelike granulomatous lesions in the bone. Clinically, sarcoidosis is a multisystem disorder of unknown etiology. The musculoskeletal manifestations occur in about 20% of patients with sarcoidosis and include joint involvement, bone lesions and macular disease. Primary skeletal involvement without other organ involvement is extremely rare. Usually, arthritis is seen early in the course of the disease. Chronic disease is rare. The most frequent musculoskeletal manifestations of sarcoidosis is an acute arthritis that occurs as part of Lofgren Syndrome characterized by the combination of erythema nodosum, bilateral hilar adenopathy polyarthritis and constitutional symptoms. If we apply our acronym and discuss the radiology findings, we find that the articular changes consist of erosions, sarcoid bone lesions can be permeative or moth eaten. Lytic or sclerotic. These lesions are very distinctive joint, space narrowing is rare. The distribution typically involves multiple joints with symmetric distribution. This is an unusual distribution as seen in the diagram. In the hand. Sarcoidosis usually involves the index and long finger joints in the skeleton. The shoulder and the hip are frequent sites. Otherwise the skeleton, the knee, the ankle and the hind foot can be but are rarely affected. There are a wide range of manifestations and thereby also many clinical and radiographic manifestations. The soft tissues demonstrate dactylitis and myopathy, lacelike granulomas are associated with sarcoidosis. These may be seen in multiple bones as we see here involving the proximal and distal interphalangeal joints of the index and the long finger. The osteolytic lesions are quite typical and described as having a lacelike or trabecular pattern. This presentation is somewhat of an Aunt Minnie because once you have seen it, you will recognize it when you see it again. This image shows an osteolytic lesion in the distal radius. Demonstrated by the blue arrow with trabecular and cortical bone destruction. In a patient with sarcoid, there is osseous destruction on both sides of the interphalangeal joint of the first digit with extraosseous extension of granulomatous tissues noted by the Black Arrow. Since neuropathic disease affects the joints, especially in patients with severe diabetes. This is an important topic for you to learn and be able to recognize neuropathic arthropathy. Also known as Charcot arthropathy is a progressive destructive joint disorder in patients with peripheral neuropathy with loss of pain, sensation and proprioception in the foot, ankle or hands. Patients with this disorder may experience fractures and dislocations of bones and joints with minimal or no trauma. The most common cause is diabetes mellitus, which typically affects the tarsal and tarsal metatarsal joints. Arterial wall calcification is commonly seen in these patients. Other causes are tertiary syphilis, also known as tabbies, dorsalis, Syringomyelia, leprosy and sometimes but rarely CPPD crystal deposition disease. The arti the articulations in neuropathic arthropathy show no evidence of erosion in the early phase of neuropathic arthropathy. The bones demonstrate inflammation and osteopenia. Finally, joint destruction with the presence of loose bodies occurs, fragmentation and insufficiency fractures when Charcot foot is treated and becomes less active, bone will coalesce with formation of osteophytes and bony proliferation. The cartilage demonstrates joint space narrowing with alkalosis. The distribution is primarily in the midfoot. As seen in the diagram. The extra findings include neuropathy and vasculopathy. The soft tissue findings include soft tissue swelling, severe joint malalignment leading to rocker bottom deformity of the foot. These radiographs are of two different patients with diabetes and neuropathic arthropathy. In image A, we see destruction of the tarsometatarsal joints with periarticular LCEC. In image B, we see typical radiologic changes in the foot of a diabetic patient. There is lateral subluxation of the tarsometatarsal joints, also known as the Lisfranc joint. The changes in bone and joint may mimic severe osteoarthritis, severe inflammation and septic arthritis or all of them together. The key in this case is the clinical history with the presence of diabetes mellitus and diabetic neuropathy. Here we see a nice example of rocker bottom deformity. This weight bearing lateral view of the foot demonstrates the dislocation in the tarsal metatarsal joints and is better visible here than on the AP view. Diabetic hand syndrome are the changes that occur in the hands in patients with diabetic neuropathy. The diabetic hand syndrome is the inability to use the hand because of contractures and stiffness. It can affect the proximal and distal interphalangeal joints and metacarpophalangeal joints and is often painless, prolonged, hyperglycemia is thought to result in the accumulation of advanced glycation end products in these regions. These glycation end products can break down collagen and deposit abnormal amounts of collagen in connective tissue around the joints, resulting in stiffening and hardening of the joints and the surrounding skin. If we look at the images, we see destruction of the carpal metacarpal joint at the base of the thumb and in all the distal interphalangeal joints, we also see erosions and bone destruction adjacent to the interphalangeal joint of the index finger and the distal interphalangeal joint of the long ring and fifth fingers and the proximal interphalangeal joint of the ring and fifth fingers. Subluxations are also present. Notice the extensive vascular calcification noted secondary to diabetes, mellitus type two. The hand of this patient with neuropathy shows the status after removal of the trapezius bone indicated by the light blue arrow. There is destruction of all the distal interphalangeal joints and erosions adjacent to the proximal interphalangeal joints and metacarpophalangeal joints. There are also erosions and bone destruction adjacent to the interphalangeal joint of the index finger and the distal interphalangeal joint and proximal interphalangeal joints as well. Subluxation and dislocation is also noted. Now we move on to hemophilia which can cause extensive changes in the joints that resemble osteoarthrosis. But the pattern is unusual hemophilia is an inherited coagulation bleeding disorder, which is mainly X linked recessive and therefore, for occurs almost exclusively in males. About 50% of the hemophilia. Patients develop hemophiliac arthropathy. This results from recurrent hemarthrosis which leads to synovial hyperplasia. Chronic inflammation, fibrosis and hemosiderins. It is frequently mono or oligoarticular early prophylaxis. With coagulation factors considerably reduces the musculoskeletal complications in the joints. In hemophilia, we see erosions and eventually joint destruction. The bones demonstrate subchondral cyst formation, periarticular osteoporosis, which is mostly secondary to the hyperemia. Ankylosis may occur in late stages. Joint space narrowing is noted and destruction in the late stage of the disease may occur. Hemarthrosis affects the large joints and is frequently mono or oligoarticular, affecting the wrist, knee, ankle and elbow joints less frequently. It affects the glenohumeral joint, sacroiliac joint and hip joint because this is an inherited disorder growth abnormalities may occur, soft tissue swelling is also present because of joint swelling or extraarticular hemorrhage please remember that when finding, look, look like osteoarthritis but are in an odd presentation or distribution in a male patient. Think about hemophilia. Here we see radiographs of the knee in a patient with a history of hemophilia and repetitive hemarthrosis distension of the suprapatellar bursa of the right knee is noted secondary to haemarthrosis indicated by the black arrow. There is narrowing of the medial joint space caused by cartilage destruction and secondary osteoarthrosis indicated by the white arrow subchondral bone cyst formation below the intracondylar ambulance is also noted and no erosions are present. As you can see, this picture is like osteoarthrosis. So it is important to have clinical history in these cases. The Arnold Hill Gartner classification is a plain radiograph grading system for hemophilic arthropathy of the knee. Stage zero is normal. Stage. One demonstrates no skeletal abnormalities but soft tissue swelling is present. Stage two, demonstrates osteoporosis and overgrowth of the epiphysis, no chondral cysts and no narrowing of the joint space. Stage. Three demonstrates early subchondral bone cyst squaring of the patella widening notch of the distal femur or humerus and preservation of the joint space. Stage four, findings of stage three but more advanced narrowing of the joint space. And finally, stage five demonstrates fibrous joint contractures, loss of the joint space due to cartilage destruction, extensive enlargement of the epiphyses with substantial disorganization of the joint. Here we see ap radiographs of both knees in a patient with a history of repeated hemarthrosis caused by vascular malformation which is not visible on the radiograph. The image of the right knee shows joint space narrowing, subchondral cyst formation and erosions of the medial and lateral tibial plateau. A normal left knee for comparison is noted here is a more typical case in a patient with long term history of repetitive hemarthrosis. Because of hemophilia, we see a slightly widened intercondylar notch on the left, which can be also found in juvenile rheumatoid arthritis and tuberculous arthropathy. The femoral condyles are bulbous with flattening condylar surfaces. The bone deformity on the left side can also be seen in tuberculous arthropathy. As a note, this is stage five, Arnold Hill Gartner classification of hemophiliac arthropathy. This demonstrates severe joint space, narrowing, subchondral cyst formation and erosive destruction. This image is of the shoulder in a patient with hemophilia and recurrent hemarthrosis of the shoulder joint. There are features of secondary osteoarthritis with subchondral sclerosis and osteophyte formation at both sides of the glenohumeral joint. In general, hemophilia arthropathy has similarities with osteoarthritis, as we stated earlier. However, the presence of erosions, extensive subchondral bone cyst formation and the history of recurrent hemarthroses are distinctive features in favor of hemophiliac arthropathy in this radiograph of the ankle on the left and a magnified view of the same joint on the right. In a patient with hemophilia, the findings include extensive symmetrical joint space loss, subchondral bone cyst formation and erosive changes here is a nice representation of endstage hemophilic arthropathy of the elbow. In this ap and lateral view, we see symmetric joint space, narrowing, joint effusion, subchondral cyst formation and secondary osteoarthritis with osteophyte formation. Although the findings themselves are not that specific, you can see the similarities in all the above cases. Chronic recurrent multifocal osteomyelitis is an unusual condition which demonstrates multifocal areas of sterile bone inflammation. Clinically. This is an uncommon autoinflammatory disorder of bone in Children and young adults that is characterized by nonbacterial osteomyelitis. Patients present with episodic m multifocal bone pain, secondary to sterile osseous inflammation. The disease has a relapsing and remitting course. The cause of this disorder is unclear. The diagnosis is made by exclusion and the main causes to be excluded are neoplasms and infections. It is sometimes diagnosed along with inflammatory bowel disease or psoriasis and there seems to be a genetic component. If we look at the diagrams, the findings are really rather unusual. The mandible and the clavicle are frequent, frequently affected as are the elbows and knees and ankles. The pisiform joint is affected in the wrist, no other joints are affected in the hand or wrist and there is no foot involvement. There are no articular findings in this disorder. The bones demonstrate first lytic lesions and then bone edema later progressively. Sclerotic lesions develop in the metaphysis along with periostitis. The cartilage demonstrates no abnormal findings. The distribution is as in the illustration, often symmetrical and multifocal typically the medial clavicles and tibia are involved. Other common sites are ribs, the mandible, the pelvis and vertebral bodies. Extra findings occur in Children and adolescents with an average age of onset of 7 to 14 years and the female to male ratio is approximately 2 to 1. So therefore, it's twice as common in women as it is in men. The soft tissues demonstrate edema around the regions of inflammation. Here we see cortical thickening sclerosis and bone enlargement of the diaphysis and metaphysis of the right clavicle and the metaphysis of the left clavicle. A spectacular spect CT and bone scintigraphy. In the same patient demonstrate abnormal radionuclide uptake and the corresponding areas reflecting increased bone turnover. This patient demonstrated pain on the left side of the hip. There is subcortical osteolysis lateral to the proximal femur demonstrated by the Blue Arrow. The MRI study below includes axial and coronal T one TS EFS sequences with contrast shows a region of bone and soft tissue enhancement about the left hip. This was found to be because of noninfectious osteomyelitis with extraosseous extension. There is also a secondary small lesion visible in the dorsal aspect of the major trochanter on the right. Our final disorder in this lecture series is Sappho syndrome. This is a syndrome that consists of synovitis, acne pustulosis of the hands and soles of the feet, hyperostosis and osteitis and is an uncommon inflammatory disorder of bone joints and skin. The pathogenesis of sca of Sfo Syndrome is not well understood. It is sometimes described as an autoinflammatory disorder. If we look at the radiographic findings and apply our mnemonic, the articular findings include joint erosions and erosion at the vertebral body corners. The bones demonstrate osteitis which is bone inflammation seen with sclerosis of the medullary cavity and bone marrow edema, hyperostosis is seen as cortical thickening formation of osteophytes, paravertebral ossification and ankylosis osteolysis is also a common finding and may lead to vertebral body collapse. The cartilaginous changes include joint space narrowing. The distribution is asymmetric including the anterior chest wall, which is the most common site of involvement. Then the mandible and spine and less frequently the cervical spine and sacroiliac joints. The extra findings for this disease is that it is seen in an average age of 30 to 50 years. Again, with a female, predominant soft tissue changes include acne and pustulosis of the palms and soles. Although skin and osteoarticular manifestations do not necessarily coexist. An important point in this disorder is that the degree of inflammation determines the type of bone abnormalities. Osteolysis will occur when there is extensive inflammation, increase of bone activity and sclerosis will occur when there is less inflammation. Here we see three different images of the same patient notice on the sagittal ct on the left that there is osteitis of the sternum and manubrium sterni with sclerotic thoracic vertebral bodies, some endplate erosions and paravertebral syndesmophyte formation. The middle image is a lateral view from a nuclear medicine. Bone scan, increased activity can be seen in the sternum indicated by the black arrow and in the mid thoracic spine indicated by the yellow arrow. The right image is an axial ct of this patient demonstrating sclerosis in the manubrium stern eye. Here is a good example of hyperostosis in Saho. This patient has extensive hyperostosis of the medial side of the clavicles bilaterally. In the ct of the same patient. We see extensive hyperostosis of the medial side of the clavicles and sternum ankylosis of the sternoclavicular joints and the 1st and 2nd sternocostal joints is also noted. We have come to the end of the arthritis lecture series on this slide. You will find comprehensive table demonstrating all the findings seen in all the diseases we discussed. It might be helpful for you to come back and photograph this table and keep it in your telephone for reference. Virtually. Everything that we talked about over the three lectures are included here. Thank you so much for your attention. And I hope you find this last lecture of three interesting and enjoyable. Any questions? Everybody's happy. Fill out your uh forms, please. And we will there. Now we stop presenting. Is that rhea still here? Yes, there aren't any sure. Sure at the moment. Dennis. Ok. That's fine. And if there's gonna be some comments, we can wait a moment, but we've stopped presenting. So and you'll of course, send me the uh statistics. Yes, super. So I guess we're done for the day. Huh? Yes. Um let's just see if anyone has any questions, but I, I'm not really convinced there's going to be many if there are. Um, thank you so much, everyone. Go ahead. Sorry. That was all I was gonna say. These are difficult topics and I'll do lectures about them all in the future that are very complete, but most of these topics are a lecture, you know, or a 30 minute lecture on their own. But we just wanted to cover them for completeness. So, are they still hearing me or not? Um, they can still hear you. Would you like me to take us off live? Sure.