 Dr. Sridhika Ghosh from Apollo Multispeciality Hospital, Skolkata. After a long hiatus, I am back here today with my tutorial. But this time, I'm going to do something different. I'll tell you six stories. No, they are not detective or horror or funny stories. They are clinical, pathological, radiological stories. Now, what do I mean by that? I'll be telling you six case scenarios from where you have to pick up the clenching factors from the history, clenching factors from the lab investigations, and the clenching factors from the radiographic features that you see, and couple it to make a clinically relevant report, which is going to completely stand out from the rest of the crowd. Hope you like my tutorial. They'll be based on metabolic hematopoietic and endocrine disorders of the bone. The first tutorial is based on my first two stories. If you like it, please subscribe to our channel and tell your friends to do so too. Thank you. We start this session. This is going to be on metabolic hematopoietic and endocrine disorders of the bone, a cased base review. The entire thing is divided into three separate tutorials. The first tutorial will be dealing with the first two case scenario. The scenario number one, a 42 year old patient, a female patient comes who has a history of surgical menopause, a total abdominal hysterectomy and bilateral sulping or uferectomy done for some purpose five years back. She comes with the complaints of polyarthritis, rash, recurrent mouth ulcers, and Reynolds phenomenon. What is Reynolds phenomenon of feeling of tingling, numbness, and cold in certain extremities, especially the fingertips, etc. Out of the various lab tests that were asked for, what stood out was anti-nuclear antibody positive. Anti-nuclear antibodies is what it indicates autoantibodies which are mistakenly being formed attacking the healthy cells of the tissue. That is, she is having some autoimmune disease. C3C4 was low. There is a deficiency in the complement system and DSDNA that is anti-double stranded DNA is quite high which is classically confirming active lupus erythematosus. I mark active lupus erythematosus. So the patient was started on pulse methyl prednisolone and followed by oral long-term steroids. Now when subsequent follow-up she comes to the clinician and now the clinician is quite surprised. She has typical cushingoid habitus. How is it like moon face, buffalo hump, truncal obesity indicating long-term steroids but she has come mainly for two things left hip pain and back pain. The lab parameters now show nothing grossly abnormal and the vitamin D was quite surprisingly normal. ALP was mildly raised. A DEXA scan was asked for her and what is DEXA scan? It is an imaging test that measures the bone density. A T score is given anything below minus 2.5 and minus 2.5 is the cut-off. Anything above that minus 3.6, 3.8 these all indicate that she is having severe osteoporosis in these regions. So the spinal area had a T score of minus 3.6 and the left hip had a T score of minus 3.8 suggesting severe osteoporosis. What were the radiographic findings? Now the central part is what the radiograph of the patient was. I have kept a normal one over here and a magnified view of the vertebral body over here. This is the normal vertebral body. This is the normal radio density of the vertebral body. This is the radio density and the thickness of the end plates. But what has happened to our case? There is severe osteopenia, increased radio lucency of the bones. There is pencil thinning of the cortex and altered trabecular pattern. These vertical lines which are standing out in this vertebra shows us that what we are dealing with is an osteoporotic bone. So we are dealing with a case where there is loss of bone mass. The quality of bone is fine but the loss of bone mass is what we are dealing with and the four important radiographic findings that we see in an osteoporotic patient is increased lucency of the bone which tells us that there is reduced bone mass. There is pencil thinning of cortex. The cortex is thin, frailed out and there is preferential resorption of the horizontal trabecular because of which the vertical trabecular they stand out because of which these vertical striations come into play and later on we see fracture deformity as we will come to this. So when we are speaking of it let us see the variety of picture that we see in an osteoporotic spine. This is what a normal vertebral body looks with like crisscross of horizontal and the vertical trabeculation. This is where there is preferential resorption of the horizontal trabecular and the vertical one stand out giving a striated appearance. This is where there is anterior wedging, there is reduction of the anterior vertebral body. The posterior height is maintained so this is anterior loss of height. When there is both anterior and posterior loss of height this is what is vertebra plana. Look at this vertebra. This is an example of vertebra plana whereas this is anterior wedging. Next there is bone softening because of which there is end plate depression on both sides giving rise to what is called fish vertebra by concave vertebra and finally angular end plate fractures acute fractures giving rise to this picture. So this is the spectrum of changes we find in the vertebra in an osteoporotic spine and because of varying degree of reduction of vertebral height or fractures there is a kyphotic spine. The spine has become quite bended you know this is what happens in a markedly osteoporotic spine. Now we are coming to the pelvis which was asked what we see again there is increased lucency of bones in general. Now the trabecular pattern also is prominent now when we come to the hip we need to know about one thing especially we hardly nowadays the students they don't go through radiographs properly but this is something very interesting for students that if the trabecular pattern in a femur is actually there are three kinds of trabeculi the principal compressive trabeculi which are extending from the medial aspect of the neck going superiorly there is the secondary compressive trabeculi which go from here medial aspect to the trochanter and the principal tensile group which runs arches like this from superior to inferior ending here and the area in the middle is what is called the wads triangle which is appearing as a normal lucency. Now this wads triangle in the previous days when everything was based on conventional radiographs so much of CT scan and MRI was not there we could understand the severity of the osteoporosis by seeing the wads triangle in early osteoporosis the wads triangle the lucency would increase but gradually in advanced cases this principal tensile group of trabeculi would undergo resorption and there would be an opening up of wads triangle which made us understand that we are dealing with severe osteoporosis. So because of the hip pain and the relatively unremarkable plane radiograph of the femur and MRI was asked for because of the pain and what we see a typical ring like subcontral area over here in the femoral neck which is nothing but a classical condition that is avascular necrosis of bone and why has it occurred exactly why long term steroids result in avian people don't know but there are some evidence that probably it is a lipid laden condition which leads to ischemia and this femoral ischemia leading to this avian over here. So when we come to this end of the story we have to find out that what are the clinching factors in the diagnosis from the history from the lab and the x-ray findings and then put into our final diagnosis. So long term steroids and long term menopause means that the patient is under low estrogen level for a long term as well as steroids for the SLE because of which he is prone to osteoporosis. The lab parameters are grossly normal vitamin D is normal which points to osteoporosis in comparison to our next case osteomalacia that we will be discussing with the dexa finding of a score less than equal to minus 2.5 is classic. So our case we have a dexa score of minus 3.6. So dexa score T score of less than equal to minus 2.5. This is classic of osteoporosis and the radiological findings of generalized bone, radiolucency, cortical thinning, altered trabecular pattern, abnormal vertebral shape, opening up a board strangle is all towards osteoporosis. Avian of femur was diagnosed. So our final diagnosis was exogenous Cushing syndrome was confirmed. Now there is a twist to this story. The avian was managed medically, corticosteroids was withdrawn gradually and the patient was started on bisphosphonase. Bisphosphonase, alendronate is a type of bisphosphonate. This therapy is given it is as an anti-resorbative therapy because of so much osteoporosis to prevent that patient was put on alendronate. On subsequent follow up what happened was the SLE remained stable patient now complained of right hip pain, excruciating right hip pain after a trivial injury. Now repeat pelvis x-ray was done to this patient who had actually come in a wheelchair, can't walk at all and what do we see? Oh my, we see a through and through biophysial fracture involving both the cortex perpendicular to the line of the bone. This is what is called a bisphosphonate induced atypical femoral fracture. What happens is atypical fractures occur when because of too long alendronate there's a mismatch of osteoblastic and resorptive therapy and so this occurs. So that closes our case but just to wind up what are the other radiological features of osteoporosis? Number one, insufficiency fracture. Normal elasticity of bone is not being able to withstand the normal physiological stress. Plain x-rays usually are unrewarding there can be a localized periosteal reaction, transverse opaque colors or associated small perpendicular lucencies. Now what do we have to know that there are specific areas preponderance for this insufficiency fractures like the sacrum, medial aspect of the femoral neck, posterior calcaneum outer margin of proximal tibia and fibula scapular blade where these lucencies are seen perpendicular to the line of the bone. So see the small lucency over here this is a insufficiency fracture other areas this is a sacral insufficiency fracture. Now as I discussed that insufficiency fractures the radiograph may be unrewarding in that case the MRI does play a role they show diffuse edema in the stair sequence fluid sensitive sequence and in T1 sequence we see linear hypo intensities perpendicular to the line of the bone. In fact bone scan also plays a role see this is a bone scan showing a Honda sign this is a vertical fracture horizontal fracture connected for producing H-shaped Honda sign this is classic of stress fracture in the sacrum. Let us see a few more pictures so this is a vertical fracture over here with callus formation this is in the pubic bone this is a femoral head a certain cases of osteoporosis gradually there is loss of the femoral head sphericity and if the patient has developed avian because of steroids then there is finally collapse and secondary degenerative changes. This is a through and through femoral intracantric fracture very common in osteoporotic patients other fractures which are very common as a part of the osteoporotic fracture profile are callus fracture the distal radius fracture over here the bimallular fracture the spine fractures that I have already shown you to cover the rest of the modalities this is what an osteoporotic spine looks on CT it just shows the trabecular prominence better the thinning of the cortex there is a wedge fracture here this is how the MRI of an osteoporotic spine looks with loss of a biconcave bone over a vertebral body here and a vertebra plana here so we just finished a case where the bone quality is normal but it is deficient in amount now coming to the second case scenario a 68 year old female who is a known case of chronic kidney disease on long-term dialysis presented with a history of low backache pain over hip excruciating pain groin and sacral region there is leg weakness and on palpation tenderness acute tenderness of was found in all these regions investigations done were radiograph the ls spine and the both hips and the blood investigation what were the clenching factors again as I have told you I marked in red the clenching factors of the lab investigation or radiograph so what were the clenching factors over here the raised alkaline phosphatase level over here which indicates that there is some bony pathology going increased serum creatinine indicates that the patient must be having some kidney issue the kidney is failing low calcium low phosphoate and low vitamin d also indicates that the patient's kidneys are not functioning and because of which these kind of findings are being found in the lab parameters what is happening actually is because of chronic renal failure the kidneys are not being able to convert vitamin d3 to calcitrol the active form of vitamin d there is low calcium there is phosphate retention and because of the low calcium level the body is trying to maintain the calcium homeostasis by stimulating the parathyroid hormone to produce parathormone leading to a condition known as secondary hyperparathyroidism it is not written here the but the serum parathormone was also high in this patient this patient was also subjected to an ultrasound of the neck to rule out primary cause of hyperparathyroidism it was normal now what did the x-ray spine reveal x-ray spine revealed prominent end plate densities at multiple contiguous vertebral levels with alternate lucent dense lucent dense areas this is what is called a rugged jersey spine why is it called a rugged jersey spine because rugby jerseys have alternate black and white stripes just looking like the spine the x-ray pelvis was bizarre there was definitely reduced a lucency there was an osteopenia everywhere and focal areas of bizarre sclerosis here and there and a chest radiograph of the same patient revealed resorption of the clavicular end of the bones both the clavicles and a careful viewing there was found to be soft tissue calcification also if we find over here in this lip so what do we have in mind we are dealing with a case of a chronic kidney disease the kidneys have failed because of which there is low vitamin D leading to osteomalacia and the low vitamin D low calcium level has stimulated the parathyroid glands to produce parathormone and because of which we have findings of secondary hyperparathyroidism so it's the spectrum of findings of both osteomalacia and secondary hyperparathyroidism first let's go to the osteomalacia part what is happening here there is a softening of the bones there is defect in bone mineralization the bone is adequate in amount but not good in quality because of the inadequate levels of available phosphate and calcium very defective osteoid has been is being laid down in the bone resulting in soft bone so what are the classical radiographic pictures there is diffuse osteopenia because of the demineralization minded not because of the reduction in bone mass because of the demineralization like an osteoporotic pattern we have coarsened trabeculae the trabecula rather have a fuzzy outline because of the abnormal osteoid being deposited on the trabecula there is loss of cortical definition so these features are kind of overlapping with the osteoporotics area but insufficiency fractures or pseudo fractures losers zones are more common in osteomalacia than osteoporosis plus because of the softening of the bone deformities are more commonly seen in osteomalacia plus obviously the history will tell us and the lab parameters will tell us whether we are dealing with osteoporosis versus osteomalacia so there is generalized osteopenia there is coarsened trabeculae there's loser zones see this translucency over here this lucency perpendicular to the bone remember students whenever you see any loser zone your mind should automatically look at the other bones where commonly we see the loser zones as I've already said scapula the radius vertebia fibula the sacrum the pubic ramy so you automatically you should try to see because whenever there is one loser then the chance that loser zones will be there somewhere else also see a pubic ramus over here there's a loser zone here faint loser zones again finally we see the effects of bone because of bone softening the vertebral body have all become reduced in height with you know gradual depression see the end plates have become biconcave fish vertebra there is protrusion of the both the femurs into the pelvis with lateral indentation of the acetabulum the trifoil pelvis okay and also we get deformities like this this is a deformity known as shepherd's group deformity whenever you'll be shown such a radiograph in your exam you'll be asked other causes of shepherd's group deformity apart from osteomalacia you can find it in fibrous dysplasia osteogenesis perfectus so the differential diagnosis should be there in your mind without any hesitation you should just tell them all the differential diagnosis and as a result of secondary hyper parathyroidism let's see what are the findings and why they occur number one bone resorption the osteoclasts are stimulated by the parathormon and they particularly stimulate the inner periosteal layer giving rise to sub periosteal bone resorption which is very typically seen in the second and the third digit the radial margin of the middle and proximal phalanx here there is very irregular margin of this particular site this is secondary to secondary hyper parathyroidism this is nothing but sub periosteal bone again look at the sub periosteal bone is and how fuzzy the margin over here is and if we see the same patient also has an area of lucency over here expansion light equation this is nothing but a brown tumor what is the brown tumor it is a localized increased osteoclastic activity and fibroblastic proliferation mimicking a neoplasm but if we have a proper history we know the biochemical parameters see other features of hyper parathyroidism we will not mark this as a neoplastic etiology and we will call this a brown tumor another finding is diffuse bone sclerosis which happens in renal osteo dystopia why does this happen this happens because of the anabolic effect of supra physiologic amount of parathormon on bone metabolism because of which there is disproportionate osteoblastic activity i have already showed you the original picture of ruggard jerseys spine similarly there can be gross osteosclerosis everywhere in a case of renal osteo dystopia this is the case of fuzzy outline of the margin of the calvarium because of abnormal osteoid soft tissue calcification is very common in secondary hyper parathyroidism also vascular calcification is quite common again we see loser's zone one over here and brown tumors look at this expansion light equation we have to remember just like loser's zones if we see brown tumor in one area we may expect to see it in many other areas we should not be mistakenly calling this a neoplasm so when we are winding up the second case again let us look into the clenching factors what are the clenching factors in the history a chronic renal failure patient on long-term dialysis with bone pain what are the clenching factors in the lab parameters raised alkaline phosphatase which is explaining some bone issues happening race serum creatinine explaining kidney failure low vitamin d low calcium high phosphate all explaining kidney failure and a raised parathormone because the body is trying to maintain calcium homeostasis and has stimulated the parathyroid glands and the radiological findings of bone sclerosis loser's zones soft tissue calcification an additional finding of USG neck normal with no parathyroid tumors point out that we are dealing with secondary hyperparathyroidism so in this tutorial we discussed about two case scenarios and two entities one being osteoporosis where the bone is thin there is too little of it though the composition of the bone is perfect and in osteomalacia where the total mass of bone is normal but it is very bad in quality it is soft weak because of poor mineralization in children this osteomalacia is known as rickets so this is where I come to end of my first tutorial my first two case scenarios my basic idea was not only to discuss the radiological features of these two as radiologists but to make students understand that instead of just reporting the findings if we go back to the history take out the clinching factors from the history make a little effort in finding out the biochemical parameters also and put everything together then instead of just giving a general diagnosis of osteoporosis or osteomalacia we can give a clinical diagnosis and I can tell you that if you give a clinical report like this taking all the pain not only will it help in your exam but even in your day to day life where your report will definitely stand out amongst others hope you like this video and after this video residents please go back and start reading your radiographs in this fashion by exploring the clinical part and have fun bye take care