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Good evening. Thank you for being with us. Always sorted out some tech issues. Uh Welcome to this evening, which is the second part of the asset essential pathology for surgeons in collaboration with the Pathological Society. Uh Tonight, we'll run into different sessions. So the first session will be a soft tissue and bone pathology with Dr Saroyan. Well, then have a short 10 minute break and then we'll move on to the next session which will be essential pathology related to breast. And these presentations are designed to help anybody and sitting there, mrcs examinations and they're also quite useful and contain practical information for day to day clinical work. We will have a chat function. So there's a chat box to give any questions which will end very kindly, the man's by doctor visit India from the Pathological Society and for any questions that we can't get to throughout the talk and we'll either answer them at the end or provide you with an email link. Um So without further g uh I'll hand over to doctor Statin who will be providing her lecture on skin, soft tissue sarcoma and bone pathology. And I hope you find it useful. Okay. Hello everyone. My name is Johnson. I'm ST three pathology training from uh Edinburg. Uh Thanks all for joining tonight and apologies about delay. Uh Tonight, I will cover a broad area uh of skins of tissue and bone pathology. Uh I'll try to fit this in our, hopefully, I will be successful. Um Julian if you move to the next slide. So the plan for tonight is I'll start with introduction um to general pathology and have you approached uh specimens and then I will cover some areas um in skin pathology, uh soft tissue sarcoma pathology and it will uh an hour line with bone pathology. Um So, um I wanted to make this a bit interactive, but unfortunately, I had some tech issues. Um So uh it is going to be more uh less interacted, interacted than I was expecting it to be. Um So I want to start with the types of specimens we received to the pathology route lab. So, first of all, we receive core biopsies. These are the diagnostic specimens. Usually they're not uh they're, they're, they're done for treatment uh planning. Uh And then we usually disc uh make diagnosis on these and discuss these cases on M D T s. Then uh following the indicate discussion and treatment planning, we receive the usually the excision specimens. These are there are different types of excision specimens. Some of them are wide local excision which are, which which which we see um most often uh this is basically basically the lesion at the uh bottom of the image. And within the uh in the wide local excision, there is like some background tissue with it. So we can assess the margins and margin clearance in this specimens somewhat, sometimes due to the cosmetic reasons or other functional reasons that we receive marginal excisions. And this is usually the clearance is quite close to the uh to the resection margin. So sometimes this can cause issues or sometimes uh unfortunately, but we sometimes see interregional resections. Um And these ones are usually like the March, there's margin positivity in these ones. Um Sometimes with benign lesion's, um we are sent piecemeal or created excisions which the lesion is removed in pieces. Uh Usually this is a case with the fibroma of uterus. Uh There's no uh these are usually benign lesion's. Um Next slide is bon tumor sections. These ones are done for osteosarcoma or viewing circumcise. Um These are like these come but usually the associated soft tissue because the usually the the uh imagine of soft tissue uh surrounding the bone is important in these lesions for assessments. So we we uh sample these throughly. Uh we usually use bands so to uh section these uh next time we see an amputation specimens, these are usually like uh the extremities or um somebody who are said lost their function due to the disease. It's and um this is a specimen these days. Um So the next slide, uh the pathology usually include in uh contains. So we make a diagnosis, benign versus malignant and give the subtype and classification of the disease. Uh We use molecular studies, eliminates the chemistry to be as specific as we can. And then we have uh we do the grading and staging. Uh We assess the margins and not give margin clearance and try to give some additional prognostic information. So, uh next slide uh so the, the first slide we receive is an H any. So it had a toxin is and stains. Uh we usually use the conventional microscopes. But on the right hand side, you see our new digital pathology workstations where we have access for me mission in cells or tissues. Uh So, and these are like, for example, this certainly Minister chemistry stain and it highlights the cytokeratin is a molecule that uh that is present in the cytoplasm of the cells. And this uh staying basically goes and attaches to the psycho keratin's and highlights epithelial cells or um within that tissue. Uh So that's some uh enemy chemistry method that we use under thousands of different stains. Um And sometimes, and now we're entering the next slide, please. Uh Gillian can I can't see the slide? But is it, oh, you should be seeing the immunohistochemical tree right at the moment. Um I can't see it on my screen. But if it is there, that's that should be fine. Uh Sorry about this. Uh huh uh Julie and I, I can't see the this like you're sharing at the moment, but if it is the molecular classification sarcoma and that's fine. So now we're onto molecular classification of sarcoma. Okay, great, thanks. So this is another technique that like recently uh like it's quite um a festival upping area. Um A little classification of the tumor's. Uh so like there are so many like new papers every day. And this is another area that uh we try and comment on if the we have facilities available in the in our trusts. Uh uh Next slide please. Great on stage. Uh This is um uh something we try to we recommend on our report in wide local excisions and tumorous sections. So great grading refers to the level of differentiation of the lesion. So, um high lesion's are mostly like or poorly differentiated lesions show appearances towards the scam cells and tend to have high mitotic count. Um This is another way to predict the risk of metastatic potential. Uh So, when we are assessing each tumor has its own grading system, uh but the main things we look at are the pleomorphic is um high nuclear decided plasma ratios and um mitotic index from you're referring to grading on left hand side. In this picture, you see on the left side of that picture, you see a chondrocyte, a well differentiated Condra uh lesion, whereas there's a demarcation line. And on the right hand side, there is a highly pleomorphic lesion that is very different from the the lesion is originating from the cells, how higher nucleocytoplasmic ratio. And um there are some methodic figures when you look at it in the high power. Uh so like the left hand side is a well differentiated, low grade tumor. Whereas on the right hand side, there is a high grade, poorly differentiated tumor. Um uh We, we want staging. It is a way to describe the size of a cancer and whether it has spread to nearby lymph nodes or to other parts of the body at the moment, TNM eight is currently uh and use. Uh so and this is uh the kind of use radiological data to give the TNM um staging because if there's a fantastic metastasis, then that upstage the tumor, obviously. So we need radiology's input um to make the final call. Uh next slide, please. Uh So here you see the uh TMM staging for uh malignant melanoma. So tea is this uh in Melanoma. It is um mostly the thickness of the tumor than the size of the tumor. Uh So the T is defined with as the, with the uh thickness of the tumor very uh and is the number of specific notes. So if the, if the lymph node, the lymph node is positive, then we then they go and do the lymph node clearance and then uh we see how many of them are involved and um is the metastatic. Uh This, this, this is metastases status of the lesion which is mostly assessed with radiology. Um So now I will move on to the skin pathology part of my talk. Uh So next slide is basal cell carcinoma. Uh So it'll cell carcinoma is the most common malignancy in humans. It is a locally aggressive tumor um and destructive, but it has a very low metastatic potential. Um It's usually it's related to UV exposure and seen in the a lighter skin people more mostly. Uh but if a person that gets diagnosed and it gets multiple BE CCS at young age, uh we think about Garland syndrome and uh the other name for this is based on cell nevus syndrome. I think this is uh this was one of your previous questions. Um So the clinical presentation is usually, uh you can see in the image is a purely popular in sun exposed areas. Uh Sometimes it is associated associated with central and um uh central telangiectasiae tick vessels and it has emerged edges, sometimes we see ulceration. Um We will discuss, we'll talk about squamous cell carcinoma and melanoma as well. But some of those lesions also present um very similar, like very similar to this. So, a local excision and sometimes biopsy is advised. So it's obviously uh done and done in microscopy. We see these nests of basil I'd cells increase nucleocytoplasmic ratio in dermis. Uh and um peripheral policy side saving is the most important feature by that. I mean, these um cells that are at the edges of these uh little nodules and they are, they look like pick it funds. Uh There's cleft formation between tumor and the surrounding Strama. These are kind of the buzzwords. Uh These are the words we use to describe these lesions. So it might appear on your exam. Um So the mutations rise BCP 53 patch one uh mutations and the treatment is wide local excision. Um Next slide is uh squamous cell carcinomas. Um So this is the second most common form of skin cancer. It is, it has a metastatic potential. Um So they, they usually appear as a red bumps, scaly patch or non healing ulcer. Uh and this is also associated with sun exposure. Uh And with this one, we see a typical squamous cells uh uh that originate from epidermis and invade dermis and we expect to see evidence of screams differentiation in terms of characterization and intercellular bridges. So, uh when you make this diagnosis, obviously, we give a stage by measuring the size of the tumor and the depth of the invasion. And then following that, the treatment depends on this assessment and usually excision and sometimes radiation. Um Next slide is um uh about checked a Gnaeus Melanoma. So I just decided because they're obviously you feel melanomas or mucosal melanomas, which I won't be discussing in this talk. Um So uh attorneys Melanoma's are they arise from melanocytes in the skin. Melanie size are in a healthy skin are based that basal layer and um they, they secrete the melanin pigment and give color to the skin and protects the uh epithelial cells from the UV light. Uh The ultra ultraviolet exposure is the main theological factor uh for continuous melanomas. But there is a familial melanoma gene that is recently identified. And this is C D K and to a also some other. Um so kids graph and Razz mutations are also reported in uh certain types of uh certain types of melanomas. So clinical presentation. So there are different subtypes for melanomas and the presentations differs from uh subtype to subtype. But usually it is a symmetrical mall with irregular borders and it's usually uh multicolored and larger than six millimeter. Uh So here you're seeing this image, uh an example like a potential melanoma. Uh So this is probably gonna get an incisional biopsy. And uh and then uh if the Melanoma diagnosis confirmed by pathologist, then they will go and do a wide local excision this month. Uh But there are different types of melanomas, um like lentigo malignant. This is seen usually on faces of the sun exposed areas. Um in elderly people, superficial spreading melanoma. This is the most common one. Uh And this one is uh uh it's like it's mostly present as a mole with irregular pattern. There's a plastic, this can be a melon ascetic. So this can be just like, this can look like a scar tissue on the skin. Uh So this is quite a tricky one to diagnose clinically. Uh Melanoma is seen at palms of the hands soles or defeat or nail beds. Uh and not a little melanoma's are more mostly lumpy and blue black in color. Um Next um Next slide is uh so like there are so many different types of Melanomas and the microscopy description and the appearances differs from type two type obviously here. But in this image, you see a superficial spreading one. So these, you see these nests of a typical Melanie sites that has melanin pigment in them. And as I told before, they are, they usually sit at the basement membrane. Um But here you see, they are kind of migrating to towards the super surface where at the top you see the carrots and layer and there's like that's a, that's a typical thing for millen site to do. And when you look closely, you see some mitotic figures. So this is a type of uh this is a superficial melanoma. So in the next is the chemistry wise be is Melanie socks, tan and S 100. And uh when we make this diagnosis, uh this is followed by white surge cliff excision. So the most important diagnostic criteria in Melanomas is the breast love thickness. Um So like they, they start of the wide local excision also depends on the breast, breast of thickness. Uh So, uh you can see here uh the safety skin margins uh and also the, the patient's get sentinel lymph node biopsy. And it is, if it is reported positive, then they go and do the lymph node clearance in recent years. Obviously, these targeted therapies are quite um uh becoming really famous and important. And uh so there there's been so many different clinical trials and recently members lose them up. It's like which is a PD L1 inhibitor and impella moba, which is a C T L A for uh blood and an antibody. Dallas uh CTLA for blockage have been shown to be really effective. And I think it was in your exam as well. And um um and also sometimes inter parents are also used as a as a treatment option. These are reserved for stage three melanoma. So the Melanomas that has metastasized to elsewhere. Um next slide. So the prognostic factors in Melanoma we are including are in our reports are tumor thickness, uh take a breath love thickness level of two tumor information. This is the clerk level. Uh if the lesion is ulcerated or not, uh the histologic subtype and the U C magnetic rate and lymphocytes and lymphocyte reaction to the to the lesion. If there are more lymphocytes, that means um that has better prognosis, microsatellites are also important because actually presence of microsatellites shows us the lymph node involvement. Um The patient related factors are age and gender young is favorable and female gender is favorable. Um So here I included the description of micro satellite satellite metastases and in transit metastasis because I was looking through some books, uh exam prep books and I think there was a question about this which I found quite niche. Um So that's why I included in my presentation. Um So microsatellite metastases mean that uh it is only can be seen under microscope and uh we can they be seen separate melanoma cells next to the primary tumor, uh satellite matthiessen's. On the other hand, they are away from the primary team still within two centimeter area. And in transit metastases mean melanoma has spread to an area more than two centimeter away from the primary tumor. But before the nearby lymph nodes so safe, they had a lower lake lesion and the regional lymph nodes would be the inguinal lymph nodes. But having a melanoma in the Thai would make it an in transit metastases. Um um That's why I included this um next next slide, please. Um So softy sheet. Now I will move on to soft tissue sarcoma. Sorry, this is, this is really quick, but I hope it will be useful for your exam. Uh So soft tissue sarcomas are, it's a very broad area. And when I was going through your questions, I didn't come across to uh like that many questions about soft tissue sarcomas. Uh Maybe I'm wrong. That's why I didn't like go in very, I didn't, I didn't include many details. Um These are very rare and I think uh you would only see these if you're working in a sarcoma center. Um These are malignant soft tissue tumor's and they are distinguished by histological findings and the origin of the cell. Um They are mostly seen in males and they are mostly seen in patient's over 15 years old and they're mostly seen in, seen in extremities. There are over 50 different soft tissue sarcomas are recognized at the moment. But uh because of this molecular diagnostic, because of that advanced in molecular diagnostics. Uh Now, uh there are actually like hundreds of different uh lesion's with different molecular signatures. Um And uh the treatment usually depends on the grading. So if it is a low grade lesion, um the treatment would be wide local excision. But if it is a high grade lesion, the patient would, would get by local excision and radiation and chemotherapy potentially. Um And next uh next slide is uh these are the different. So when we are doing the classification of the tumor's, we use who blue books. So as and soft tissue has a blue book. And the uh here you see, you see the different classification of soft tissue sarcoma. So, Adipost stick, uh hyperplastic fibrosed ascetic smooth muscle parasite. This is the one that the cells dis originates from the cells that around the vessels. Uh skeletal muscle vascular condos is and uncertain differentiation. These are highly pleomorphic and high grade lesions that we can't identify any, any um differentiation. Um So again, tina mate is used for staging and the grading, there is a specific grading system for sarcoma is and this is uh in UK, we use French federation of cancer cancer center system. So, um there, there is three criterias with the, the first one is the differentiation. Second one is the mitotic count and the third one is the necrosis and then they get uh scored uh according to these and then uh great one is a well differentiated and grade three would be uh poorly differentiated um sarcoma. Uh Next side. So here I will quickly talk about the Romanies Syndrome. Uh So, because I've seen a question about this and uh there is, this is an autism, all dominant hereditary disorder. These patient's present with commonly present with at an early age with sarcoma. But it can also like these patient's also have breast carcinomas or lymphomas, leukemias and some adrenal glands, lesion's as well. Uh So, the mutation in p 53 gene drives this disease process. And obviously, they, when they diagnosed the whole family goes through this uh genetic testing process, um they get referred to genetics. Um um Now I'll jump to bone pathology. Uh Here, I will quickly talk about uh the normal bone histology uh because we will have um we'll see some images in following slides. Um So the bone is composed of the trabecular bone and the cortical bone and the bone marrow. Uh in adults, bone marrow is usually replaced by Oedipus sites. So, here you see the deposited tissue between the pink, pink islands of woven bone uh which are bone tropically. Let me look high power. Uh We see the adiposus that that from the deposed tissue. Uh These contain a hard really um really it, this contains fat uh like in their cytoplasm. And then this is the trabecular bone. And the how we understand this trabecular and mature bone is the collagen fibers. Uh You see that they run parallel to each other and um but sometimes some lesions or when the bone is um healing from fracture, uh the osteo osteo side osteoblasts excrete woven bone, which the, the collagen is haphazardly placed in those um in those areas. And that's how we understand that if the bone is late recently or effects, it has been there for a long time. And then there are some like uni within the Lamela bone and uh these areas contain osteo sites. Uh We expect to see osteoclasts at the, the rim of the uh the trabecular. Uh Here, I can't see any but they are there. And then let's osteoblasts. Uh uh So, next slide, uh I will talk about pathological pro uh fracture. So pathological fractures are fractures that a cure an abnormal bone and they a cure spontaneously or following minor trauma. Uh So, the causes are obviously the most important cause is metastatic tumor's uh tumors that metastasize the bone are breast, lung, thyroid, kidney and prostate mainly. So, uh for example, uh they, so they the pathology ical structure secondary to metastatic disease, most commonly appear in the proximal femur and proximal humerus. So, uh when this pathology, ical uh fracture is diagnosed and removed, the head of the femur is removed to say um that arrived to lab and then we take samples and then we run some immunised a chemical tests. Um We look at them under the microscope and run some immunohistochemical tests to see if there are any met, any matter if there's any metastatic disease in this area. Other, other causes of pathological fractures are generalized bone diseases. Uh One of which is osteogenesis imperfecta. Uh This disease presents uh the cause of the theology of this is mutations and genes that code collagen one. Um uh And I think there was a question about this as well. The it was asking about the uh the genes, this specific names of the genes. Um and the other causes are osteoporosis. Metabolic bone disease is uh and Paget's disease. Um There are some local benign conditions that can lead to um the pathological fractures and some primary malignant tumor such as condo psycho, mostly cycm and evenings tumor. Also, radiation of bone and steroid use is one of the main main causes of pathological fractures. Um Next slide, all I'll briefly talk about the process is, is obviously everyone knows here that it's a reduction in total bone mass tickles, weakening of the bone. Here you see a normal spine and you can see that trabecular um trabecula mash uh and then how it is organized and in the osteoporotic bone, um the the amount of the trabecular bone, the trabecular bone it decreases and and it becomes more prone to fractures is more common in females, especially after menopause. And um it causes fractures, italy fractures, particular neck of femur and March April. So, diagnosis um made with dexa scan uh and the vitamin d in casting levels um are normal. Um So the next slide is uh metastatic carcinoma to the bone we've discussed in the previous that slide. It's the communist tumor of bone is metastatic carcinoma. And uh we use the Minister Chemistry to identify the origin of this lesion. I'll quickly talk about multiple myeloma in next slide. Uh So this is the most common primary bone disease in elderly uh patient group. So these patient's present with bone pain, bleeding, recurrent infections and anemia. Um findings are lytic bone lesions on X ray hypocalcaemia, renal failure. Uh So we see that uh on the left hand side, you sit lytic bone lesions and spike on protein electro versus I G light light chains on in urine as well. Uh So microscopically, uh so it's usually we received to find biopsies from the bone for this and usually work with him, him past the uh hematology team. Uh So it's like it's as you see. So the on the left hand side, you see the trabecular bone and the, the, the basically the it is hilarity of the bone marrow has increased. Then there are several, some a deposit sites present. But um there are multiple plasma cells um when you look at it and the high power and they're they are distributed with an uh in an interstitial pattern. So we use some Minister chemistry again to identify the plasma cells. And if it is more than 20% of the total sell population in Bambara, then we make the diagnosis and if with the clinical findings, we make the diagnosis of multiple thing myeloma. Um Next, I will talk about osteomyelitis quickly. So it's mainly I will talk about cute. So it's acute inflammation uh with bone distraction. So, necrotic bone with uh empty osteocyte Lucchini and that we can see a brisk osteoclasts activity. So, on this image, you see that the bone marrow, uh the the the bony trabecula and there is some scalloping at the edges and that is um that is what the most most eaten pattern is and there are some empty lucky me. Uh If you look closely, you can see that there are like the empty little circles in the lamellar bone. So that is, that means that that osteo side had, had died due to the inflammation in the bone. And obviously, the bone marrow is very fibrotic. And when you look closely, there are some acute and chronic inflammatory cells present. Um So the most common causative agent is stuff like oh cause areas. Uh It's a grand positive uh Kokkai but skills sickle cell patients' might have infections with salmonella species. Um Next, uh slide talks about pathophysiology of cute osteomyelitis. So we see microbial invasion and acute inflammation. Um then this leads the race, intraosseous pressure and obstruction of blood flow to the, to the, to the rest of the bone. And then um this leads to necrosis and dead bone which is called uh sequestrum. And uh sometimes there's obviously the and suppress still abscess forms and uh this process and then that forms a little sinus track that opens to the skin. Um and then uh like after a couple of uh weeks, new bone is formed around doing uh sequestrum and this is called them all look room and and then this either resolves or if the infection continues, then this leads to chronic osteomyelitis where the acute inflammatory cells are replaced by mostly chronic inflammatory cells such as plasma cells and lymphocytes. Um So this another question I came across was squamous cell. Carcinoma can develop in this in the sinus tract that opens from the from the bone to the skin. The reason for this is obviously the chronic inflammation that is ongoing and irritating the squamous cell lining of the sinus tract. Um next slide. So um this is a, this is a case. Um uh so this is kind of a 14 year old male first experienced mild pain in the left knee after playing football, uh pain persistent in a uh intermittent fashion and uh and then approximately two weeks prior to the admission, the pain increased significantly and newly formed bone. Uh This is different than the lamellar bone that we had seen before. Uh the collagen bundles. Our if you look, if you polarizes the collagen bundles would be haphazardly arranged. And uh obviously, um uh so sometimes um that you can see mitotic figures. Um and uh like obviously, the clinical presentation is quite similar to um osteomyelitis. So, it's one of the different shows we have to consider um next slide. So, uh these are commonly found that distal femoral proximal tibia in younger people. Um And they, they are usually, they usually present with rapid progressive pain and swelling, the tumor suppressor genes uh written a blast. Um A protein and P 53 mutations have been demonstrated in some of these lesions. Um Such a also familial syndromes, likely Farrah many um can present with osteosarcoma owns and next slide. Uh So nine year old male presents with an increasing pain in left upper arm of approximately three months duration and a recent onset of low grade fever. On physical examination, there was some local tenderness and soft tissue swelling over the proximal and mid thirds of the left humerus. So in in this case, is treat the most important. I think things dialogue is patient states and uh short duration of symptoms. Uh So the one of the obviously it can be a acute slash chronic uh osteomyelitis or osteosarcoma like we discussed. And the other differential is giving scars using sarcoma. So, you know, you see uh this is upside down, unfortunately, sorry. Um uh uh like the humerus and there is a lesion in the proximal humerus that extends into the soft tissues. Sorry about the low quality of this image because I had to change these slides. Uh I mean, obviously this patient gets a biopsy and then by Ewing's sarcoma is uh diagnosis uh was made and then they went back and two humerus out. And then when we cut the, uh then we see this lesion mainly situated that diagnosis of the long bone and uh this uh lesion extends into the soft tissue. Um so it can't microscopically will be uh osteosarcoma. But when we look at down in the mic down at the microscope, we see this uh team or withdrawn blue cell morphology, but it sells with very small amount of cytoplasm, very crowd id, highly mitotic lee active doesn't look like anything um similar to bone. Uh And then the other thing is it doesn't form roven, it doesn't form woven bone like we said in showing. So in the oxidase sarcoma case, uh So this is ewing sarcoma. So it's a malignant small round cell sarcoma associated with translocation 11 22. Uh This is a very famous translocation. So they might, it might come up in exam and this leads to the formation of fusion protein E W S flight one. Uh So it is commonly occurs in the dioceses of long bones in patient's less than 25 years old, usually seen in the second decade of life. Life diagnosis is made of the biopsy and the immunised A chemistry um uh like C D 99 is quite a famous uh Minister Chemistry for Death lesion. So it might come up in the exam in the case. Um So I just wanted to include it. Um uh So coming towards and I will quickly talk about chondrosarcoma is here. Uh So the country sarcomas are malignant primary bone tumor's. There are not from the osteo bone cells is from the cardiologist cells which are called chondrocytes. Uh um They are mostly seen in uh axial skeleton like pelvis, sometimes in proximal femur. Here, we seen the proximal humerus. Uh There are usually older patient's around age 40 and usually present with a progressively painful mama's. Um The histological grade is the most important prognostic factor here like other psych Omagh's and also extra compartmentalize spread and local occurrence. The molecular signature of these lesions R I D H one and I D H two imitations. This is only seen like this is seen in half of the cases. Um set. Next slide is um so it's again, uh chondrosarcoma is can be classified as primary chondrosarcoma uh which is the law which can be classified as uh there are sub classifications such as low grade, high grade and they differentiated. So this image we've seen this before. So on the left hand side, we see a low grade chondrocyte coma, which is very similar to the healthy cartilage tissue. And on the right hand side, we see this spindly spindle cell lesion which doesn't have any resemblance to the cartilaginous lesion. So if we only receive the biopsy from the right hand side, it would be really difficult to uh identify the cell or the origin of this uh lesion. But luckily, we have both sides. So, uh so that means that this is a different differentiated chondrosarcoma because we see the both high grade and low grade in the same lesion. Uh It was on only on the left that that would be a low grade and if it was only on the right and that would be the high grade. Um So there are also other secondary chondrosarcoma is that, that arise from a benign card to legislation such as uh the these benign cultural legislations are uh things like osteochondroma or Ankan dramas. They're all, there's, there are also syndromes like such as failures, disease or Med Fugees syndrome. So the incan dramas, these diseases come with incan dramas and these and like multiple Ankan dramas, especially in distal extremities and the risk of malignant transformation is quite high in these and enchondroma. So these patient's are in close monitoring. Uh So another case, um so this is a 2035 year old female presents with a two month history of right knee pain. The radiograph shows a lytic lesion with a well defined but um non sclerotic margin involving both metaphysics and epiphany sis of this long bone. And uh so in the microscopically, we see this again, a valve demarcated lesion. Uh it has a hemorrhagic appearance and almost looks necrotic uh in center um in the emphasis and benefits and the epiphysis and math emphasis of the long bone, the cortex extent. However, there is no expansion in and extension into the neighboring soft tissue. So, the biopsy shows uh one on the clear stromal cells and some back looks like fibroblasts and numerous giant cells. So the giant cells are these cells which has um multiple nuclei within one cytoplasm. So these are cells, these cells are basically osteoclasts. So osteoclasts hard have giant cell appearance. Uh So the diagnosis for this case and is in the next slide which is giant cell tumor of bone. It says a benign locally aggressive tumor's typically found in the epiphanies of lung bones. Uh So these are, these patient's are usually between ages 30 to 50 and uh females. Interesting, they are more commonly affected uh with this from this disease. It's quite unusual is usually man who gets the bone, um bone new plastic bone lesions. So, uh Minister Chemistry, um which it has a special uh Minister chemist school marker which might come up in the exam. It is Histon 3.3 as positive with this marker. And um part officially ranked pathway is important in pathophysiology of this disease. And then denosumab is a new antibody that acts and inhibits rank ligand, I think. And it is quite uh important new drug and treatment of this uh disease is uh so the other differential uh one of the differentials of this um uh entity is brown tumor of bone. Obviously, patient history here is very different. It is uh this lesion, this patient's have hyperparathyroidism uh sometimes due to secondary to renal failure. Um and they present with elevated blood calcium and pretty with hormone levels. Uh So on X ray, we see a val defined paralytic lesion's and the cortex might be thin but there there's no expansion or involvement of the soft tissue. Uh So, microscopically, we see hammer a chem acid rain and micro fractures, microscopically decision resembles giant cell tumor of bone because there's an increase of state plastic activity due to the increased parathyroid hormone levels. So um the diagnosis is usually made uh with the clinical history and clinical correlation. Uh So I think this is the end of my talk. I'm happy to take questions. Um And I apologize. It's just I had to, I missed some of the slides because I um because of the technical issues. But yeah, I'm happy to take any questions if there are any questions. So I think the chapter is currently empty. So I don't think there's any questions at the moment. Um I can't say a huge thank you for giving your talk and for giving it under the technical constraints that we had. Um I personally a lot from it and I know it would be really useful for those um sitting there mrcs in the coming months. And so that's you completely off the hook. And what we'll do is we'll give everybody a 10 minute break. And so if we meet back here about five past eight, and then we'll be joined by Doctor Lisa Johnson who will be talking us through key and pathological concepts in breast disease. But thank you again for that much for giving us your time. Yeah, thanks. Bye.