PTH and osteomalacia question

[HiddenTruth]

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Ok, so after reading Robbins for like over an hour trying to udnerstand one little concept, I have as a result, added a plethora of uselss knowlede and additional questions. So, help me understand this, if you will.

In osteomalacia and rickett's, the straw that breaks the camel's back is the HYPOPHOSPHATEMIA (which btw, I didn't know before--I always thought it was the hypocalcemia) that ensues as a result of almost complete calcium compensation by PTH, which ultimately leads to NEAR NORMAL calcium levels and hypophos-- resulting in an abnormal ca-phos solubility product-->ricketts or osteomalacia, correct??

1. Ok, so, my next question is that in chronic renal failure and secondary hyperpth, why is it that you get osteomalacia? In this case, is it because there is inadequate compensation of calcium release from bone and reabs from renal tubules? But, that doesn't make sense, because somehow in ricketts and OM, the calcium compensation is nearly complete despite vit d deficiency. In CRI, we have hypERphos, so I don't quite understand how you get OM? Unless, ofcourse, it's simply because of inadquate compensation of calcium by PTH. In Robbin's they do talk about some alluminum crap, which can increase in dialysis pts because of the dialysis solution, and that intereferes with calcium hydroxyappetite deposition, which can cause OM--but I think, there is a more accredited answer, as that seems like a "postulate". Maybe, i am thinking too much into this (damn robbins). Will appreciate some input.

2. Oh, and also, hyperphosphatemia DIRECTLY stimualtes PTH release?

 

[automaton]

well the kidneys activate vitamin D, so if you have renal failure you're not getting enough 1,25 vitD. that will cause decreased calcium absorption which leads to PTH release due to lack of negative feedback from calcium.

i don't know if this is your question but the reason why serum calcium levels are "compensated" is because you're breaking down bone. thus your bones are screwed and you get osteomalacia/ricketts.

update: i looked up http://www.emedicine.com/med/topic374.htm ...
apparently renal insufficiency decreases filtration/excretion of phosphate. thus you get hyperphosphatemia. hyperphosphatemia inhibits KIDNEYS from making 1,25 vitD. however it also says a little bit lower down that hyperphos does trigger PTH as well. go figure.

 

[phoenixsupra]

Ah, I've been looking into this today too.

1. decreased activation of Vit.D ---> decreased intestinal absorbtion of Ca causing low Ca levels.

2. This leads to a rebound increase in PTH which causes increased reabsorbtion of Ca in the kidney and from the bones. This balances the previous effect leaving us with low/normal Ca. The increased PTH also causes decreased reabsorption of phosphate from the kidney causing a hypophosphatemia that gives rise to the osteomalacia.

That's how it is in the usmleworld solution. I don't think phophate levels directly stimulate the parathyroids.

Vit. D functions to increase the intestinal absorbtion of both Ca and Phos. It doesn't control renal reabsorbtion. PTH does that directly.

 

[HiddenTruth]

well the kidneys activate vitamin D, so if you have renal failure you're not getting enough 1,25 vitD. that will cause decreased calcium absorption which leads to PTH release due to lack of negative feedback from calcium.

i don't know if this is your question but the reason why serum calcium levels are "compensated" is because you're breaking down bone. thus your bones are screwed and you get osteomalacia/ricketts.
QUOTE]

ok--your first part right, explaining the hypocalcemic stimulus for pth release; however, the seond para is incorrect. haha--you are right, your bones are "screwed" because of the calcium compensation, but that's the mechanism for OFC (osteitis fibrosa cystica--which is mainly in PRIMARY hyperPTH and in a mild form in seondary hyperPTH, in the case of CRI). Osteomalacia and rickets is a problem in bone MINERALIZATION, something regulated by phosphate and calcium levels. OFC is a direct result of calcium resorbed out of the bone by PTH. (PTH binds to osteoblasts and releases IL-1, which activates osteoclasts, etc).

So, my question is still unanswered. Why do you get osteomalacia in CRI? The obvious reasoning is ofcourse no vit d--> hypocalcemia, which impairs mineralization. However, according to robbin's, calcium levels are near normal after compensation by PTH (and no, taking calcium out of the bone does not cause OM). Actual OM and rickets is due to HYPOphosphatemia, impairing cacium solubility prodcut formation, and thus--imparied calcification of bone matrix. But , in CRI--as you stated, there is HYPERphosp. The only thing I see is that the calcium is not fully compensated, and that's the cause. I don't know. I guess this is kind of important because, if really the HYPOphosh is the direct cause of impaired mineralization, then Vit D defic of RENAL origin does not cause OM/ricketts.

2. And, although, the review books don't straight up say that hyperphosph is a stim for PTH release, there is a blurb in robbin's that does indicate that. But, I don't think it's high yield. I was jus trying to think of the mechanism of PTH release in secondary hyperPTH, other than hypocalcemia caused by defic of calcitriol production.

 

[HiddenTruth]

The increased PTH also causes decreased reabsorption of phosphate from the kidney causing a hypophosphatemia that gives rise to the osteomalacia.

Vit. D functions to increase the intestinal absorbtion of both Ca and Phos. It doesn't control renal reabsorbtion. PTH does that directly.

That's my point (first para), but in CRI--you have HYPERphophatemia.

Although, vit d has no direct effect of reabs. from the kidneys, it is a collaborated effect together eith PTH, meaning it won't happen without vit. D.

 

[phoenixsupra]

That's an interesting question. The answer seems to be that nobody knows.

"The histopathology of osteosclerosis in renal osteodystrophy is complex and incompletely understood."

That's from the above linked page. The textbooks give us the currently known pieces of the puzzle, but no one has solved the problem yet. I searched on pubmed and there's a fair bit of research going on in an attempt to solve it. In any case, since science hasn't got this down yet, then my guess is that the USMLE won't be expecting you to have solved it either. 😉

 

[automaton]

woah did not know that. thanks for the heads up bro.

 

[HiddenTruth]

no doubt, anytime bro--make sure u hook a bro up about your test experience after it's over 😉 u take it pretty soon, eh?

 

[dcpark74]

Here's my $0.02

Hyperphosphatemia promotes secondary hyperPTHism due to its complexation with calcium in serum, thus lowering serum calcium and indirectly stimulating the release of PTH. (renal osteodystrophy)

I dunno what you guys are talking about before, but it seems much is unknown about vitamin D. In chapter 9 in Robbins says a whole lot of 'unclear.'

 

[Ramoray]

Alot is unknown but osteomalacia path is not one of them! Like everone says renal failure does a few things. Hyperphosphatemia both DIRECTLY activates PTH as well as indirectly via the drop in Ca. It also caused metabolic acidosis. So in the blood you have High PTH, normal Ca and high Phosphate however bone is full of osteoid but unable to mineralize due to 2 main reasons. 1. Primarly it is the acidemia. Remember hydroxy apatite is CaPO4 OH, when you have increased acid( H+) reacts with the Hydroxy group OH and disrupts the normal ionic balance of hydroxyapatite, leading to decreased levels which DECREASE minerlization. 2. The increased levels of aluminum and other trace ions that you were unable to get rid of via the kidney (Al2+) directly competes for PO4 and therefore less Ca binds to PO4 and creats hydroxyapatite within the bone therefore again decreasing hydroxy apatite and decreasing minerlization. So those 2 things both ldead to decrease hydroxyapatitie and decrease minerlization of normal levels of osteoid, in spite of normal levels of Ca and PO4.

 

[2TIM4:7]

Alot is unknown but osteomalacia path is not one of them! Like everone says renal failure does a few things. Hyperphosphatemia both DIRECTLY activates PTH as well as indirectly via the drop in Ca. It also caused metabolic acidosis. So in the blood you have High PTH, normal Ca and high Phosphate however bone is full of osteoid but unable to mineralize due to 2 main reasons. 1. Primarly it is the acidemia. Remember hydroxy apatite is CaPO4 OH, when you have increased acid( H+) reacts with the Hydroxy group OH and disrupts the normal ionic balance of hydroxyapatite, leading to decreased levels which DECREASE minerlization. 2. The increased levels of aluminum and other trace ions that you were unable to get rid of via the kidney (Al2+) directly competes for PO4 and therefore less Ca binds to PO4 and creats hydroxyapatite within the bone therefore again decreasing hydroxy apatite and decreasing minerlization. So those 2 things both ldead to decrease hydroxyapatitie and decrease minerlization of normal levels of osteoid, in spite of normal levels of Ca and PO4.

yeah yeah yeah. 👍

2 main reasons? there are multiple reasons. ever hear of PTH activation of osteoclasts via osteoblast activation? IL-6, RANKL, etc. (btw, the aluminum origin is not from renal failure but from iatrogenic causes!)

 

[Ramoray]

yeah yeah yeah. 👍

2 main reasons? there are multiple reasons. ever hear of PTH activation of osteoclasts via osteoblast activation? IL-6, RANKL, etc. (btw, the aluminum origin is not from renal failure but from iatrogenic causes!)

Actually osteoblasts, clasts, Il 6, RANKL( both of which stimulate clasts) have nothing to do with osteomalacia, which is simply a disorder of decreased minerlization of osteoid. The increased blast-clast breakdown of bone is a cause of the High turnover problems in renal failure, such as dystrophic bone problems in renal failure but this thread was talkign about the low turnover disorders that accompany renal failure; primarly OSTEOMALACIA and its mechanism. learn your disorders you fool. ANd obviously AL is iatrogenic but with no kidney fxn how are you supposed to get rid of it once its introduced, once again try thinking a little bit you *******.

 

[phoenixsupra]

Alot is unknown but osteomalacia path is not one of them!

Actually, yes it is. But your authoritatively stated waffle is as convincing as any other that can be found. I'm sure you'll make chief medical student one day.

 

[HiddenTruth]

yeah yeah yeah. 👍

2 main reasons? there are multiple reasons. ever hear of PTH activation of osteoclasts via osteoblast activation? IL-6, RANKL, etc. (btw, the aluminum origin is not from renal failure but from iatrogenic causes!)

A little quick to jump the gun, aren't we? By the way, ever heard of that abovementioned mechanism on causing OSTEITIS FIBROSA CYSTICA (von ricklenhans (sp?) disease of the bone, and NOT osteomalacia? PTH draining calcium out of the bone does not cause OM, it results in OFC--a "brown tumor" like picture.

 

[HiddenTruth]

Alot is unknown but osteomalacia path is not one of them! Like everone says renal failure does a few things. Hyperphosphatemia both DIRECTLY activates PTH as well as indirectly via the drop in Ca. It also caused metabolic acidosis. So in the blood you have High PTH, normal Ca and high Phosphate however bone is full of osteoid but unable to mineralize due to 2 main reasons. 1. Primarly it is the acidemia. Remember hydroxy apatite is CaPO4 OH, when you have increased acid( H+) reacts with the Hydroxy group OH and disrupts the normal ionic balance of hydroxyapatite, leading to decreased levels which DECREASE minerlization. 2. The increased levels of aluminum and other trace ions that you were unable to get rid of via the kidney (Al2+) directly competes for PO4 and therefore less Ca binds to PO4 and creats hydroxyapatite within the bone therefore again decreasing hydroxy apatite and decreasing minerlization. So those 2 things both ldead to decrease hydroxyapatitie and decrease minerlization of normal levels of osteoid, in spite of normal levels of Ca and PO4.

ramoray, well said--i agree with you. I remember reading aboout the increased anion gap acidosis, which the bone is trying to biffer by releasing the Ca OHyappetite. And, indeed that is correct, because that results in osteporosis, but what is osteoporisis?--loss of mineralized bone mass. The Al theory also makes sense, but I think that may be much more prevalent in patients on dialysis, in which they apparently use some kind of Al dialyziing solution--but, yea you would think that endogenous Al also is trying to compete with phos secondary to renal failure. Overall--I think you are correct. Thanks for your help.

 

[phoenixsupra]

Yes, that was a great soup'o'theories. Don't forget to pick up your nobel prize on the way out.

 

[dcpark74]

A little quick to jump the gun, aren't we? By the way, ever heard of that abovementioned mechanism on causing OSTEITIS FIBROSA CYSTICA (von ricklenhans (sp?) disease of the bone, and NOT osteomalacia? PTH draining calcium out of the bone does not cause OM, it results in OFC--a "brown tumor" like picture.

i was just trying to tell him that there are definitely OTHER contributing factors in RENAL OSTEODYSTROPHY!!!! it is not just OSTEOMALACIA!! IF YOU READ CAREFULLY RENAL OSTEODYSTROPHY has FIVE count them 5! associated pathologies; P. 1288 robbins rev edition #7 1. osteitis fibrosa cystica (!) 2. osteomalacia 3. osteosclerosis 4. growth ******ation 5. osteoporosis.

Who's the dumb/foolish one? (Ramoray?) Oh btw, ramoray...calm down with your ego and your SUPERB 🙄 knowledge of pathology. Lemme guess...you're not truly happy with yourself.

 

[Ramoray]

geez, its not like i claimed to spend my life doing this research and here are my theories, this is what i have read in a few books and i am relaying the info. Some is from robbins like the original poster posted but then i did have the same confusion earlier in the year while doing MSK and bone path and ended up looking some stuff up to clarify and now i am just passing along what i learned since i had the same confusion. I mean look in cecils or harrisons or UPTODATE or any of those and youll find the same thing.
Oh yes about Al being do to renal solutions, that is true, i guess in my head when i think chronic renal failure i assume they would be on dialysis but i guess that wouldnt always be true huh? Your right though w/no dialysis solution the Al wouldnt be there but i am pretty sure the same can go for other 2+/3+ ions in the body as they would be competing for the PO4 ions if they were in excess but yes im sure this predominates during dialysis.

Oh yes i meant blasts, clasts, RANK etc was important for ost. fibrs. cystica, not dystrophic, i konw it has 5 parts but in your post you were saying clearly in response to my post about osteolmalacia taht i left out all those other factors.

Osteoporosis, i may be confused but i thought osteoporosis was also do to decrease blast/or increase clast levels also and a disruption in osteoid?

sorry to offend anyone by trying to help clarify a question, sheesh

 

[Ramoray]

Actually, yes it is. But your authoritatively stated waffle is as convincing as any other that can be found. I'm sure you'll make chief medical student one day.

what a tool, if i reember correctly you go to AZCOM, which i have a ****load of friends at, ill find out who you are and see if you are a tool in real lief as well which surely you are. Go study and maybe you can contribute to the posts with some actual helpful knowledge one day instead of making toolish posts and displaying that clearly you need a life.. later.

 

[HiddenTruth]

i was just trying to tell him that there are definitely OTHER contributing factors in RENAL OSTEODYSTROPHY!!!! it is not just OSTEOMALACIA!! IF YOU READ CAREFULLY RENAL OSTEODYSTROPHY has FIVE count them 5! associated pathologies; P. 1288 robbins rev edition #7 1. osteitis fibrosa cystica (!) 2. osteomalacia 3. osteosclerosis 4. growth ******ation 5. osteoporosis.

Who's the dumb/foolish one? (Ramoray?) Oh btw, ramoray...calm down with your ego and your SUPERB 🙄 knowledge of pathology. Lemme guess...you're not truly happy with yourself.

Sorry, last time i remember and checked, the post was about OSTEOMALACIA (hence the title, "...PTH and osteomalacia"), and NOT renal osteodystrophy. I agree with your comments above, but you post clearly did not clarify what you were referring to, and given the fact that this thread was about osteomalacia, I think it was reasonable to make the assumption (as did by ramoray and I) that your comment was incorrect in respect to OM. Sorry, if this has caused any serious life altering changes in people's lives. I am sure, each one of you have at least learnt something, including myself.

Seriously, are all med students like this? It seems as if most of them exist on this forum--sheesh!! 🙄 take a chill pill dude!!

I like how a simple question about path has degenerated this thread into absolutely unnecessary, and worthless personal callouts.....but, i still love you guys 😀

 

[phoenixsupra]

what a tool, if i reember correctly you go to AZCOM, which i have a ****load of friends at, ill find out who you are and see if you are a tool in real lief as well which surely you are.

No dork, you "remember" incorrectly. And with your attitude (namecalling, arrogance, narcissism etc) I doubt that you do have any friends. 🙄

Go study and maybe you can contribute to the posts with some actual helpful knowledge one day instead of making toolish posts and displaying that clearly you need a life.. later.

You need to take your nose OUT of your books a little more and learn not to be such an unbearable prick. 😉

 

[phoenixsupra]

i was just trying to tell him that there are definitely OTHER contributing factors in RENAL OSTEODYSTROPHY!!!! it is not just OSTEOMALACIA!! IF YOU READ CAREFULLY RENAL OSTEODYSTROPHY has FIVE count them 5! associated pathologies; P. 1288 robbins rev edition #7 1. osteitis fibrosa cystica (!) 2. osteomalacia 3. osteosclerosis 4. growth ******ation 5. osteoporosis.

Who's the dumb/foolish one? (Ramoray?) Oh btw, ramoray...calm down with your ego and your SUPERB 🙄 knowledge of pathology. Lemme guess...you're not truly happy with yourself.

Don't worry, you were obviously giving sincere imput in a helpful manner.

This ramoray dude, is a classic narcissist. Extreme arrogance in defence of underlying low self-esteem. Way over the top. We have a fellow like him in our class who we refer to as "chief medical student". Thinks he's a God. Doesn't know he's everyone's laughing stock. He had a rough time on rotations btw 😉

 

[HiddenTruth]

We have a fellow like him in our class who we refer to as "chief medical student".

haha, i like that--can we make it an official SDN word?

 

[phoenixsupra]

Seriously, are all med students like this? It seems as if most of them exist on this forum--sheesh!! 🙄 take a chill pill dude!!

No, but certainly enough to polute the air. Giant and extremely fragile ego's y'know.

 

[phoenixsupra]

haha, i like that--can we make it an official SDN word?

Be my guest. 😀

 

[Ramoray]

No dork, you "remember" incorrectly. And with your attitude (namecalling, arrogance, narcissism etc) I doubt that you do have any friends. 🙄





You need to take your nose OUT of your books a little more and learn not to be such an unbearable prick. 😉

Sorry dude that was a dumb comment to make anyway and i have no problems with you so i apologize for the immature comments. It just seemed a bit odd how everyone started jumping on me for answering the original posters question with knowledge i had found since i had the same problem. I dont see why that warrented a bunch of comments for answering the post? its not like i added some random irrelevent info or tried to sound smart, i told you i didnt come up with the ideas. Well anyway sorry if i caused a problem i was only trying to help the poster, I know how it feels to spend 2 hours trying to clarify something becasue a book fails to connect a few details or explain a few things. its a pain in the ass.

 

[phoenixsupra]

Sorry dude that was a dumb comment to make anyway and i have no problems with you so i apologize for the immature comments. It just seemed a bit odd how everyone started jumping on me for answering the original posters question with knowledge i had found since i had the same problem. I dont see why that warrented a bunch of comments for answering the post? its not like i added some random irrelevent info or tried to sound smart, i told you i didnt come up with the ideas. Well anyway sorry if i caused a problem i was only trying to help the poster, I know how it feels to spend 2 hours trying to clarify something becasue a book fails to connect a few details or explain a few things. its a pain in the ass.

That's ok. No big deal. Medschool can get to you, that way. It's best not to react to it. Then you can avoid becomming like that yourself. 🙂

 

[HiddenTruth]

Oh yes about Al being do to renal solutions, that is true, i guess in my head when i think chronic renal failure i assume they would be on dialysis but i guess that wouldnt always be true huh? Your right though w/no dialysis solution the Al wouldnt be there but i am pretty sure the same can go for other 2+/3+ ions in the body as they would be competing for the PO4 ions if they were in excess but yes im sure this predominates during dialysis

Yea, actually (I learnt this on my IM rotation) you don't end up going on dialysis until your cr. cl is wayy high--like >10 or so, I think (I forgot the real #). But, I mean eventually you will end up on dialysiss with CRI. But, anyways this is irrelevent. And, yea Iron can do it too

Osteoporosis, i may be confused but i thought osteoporosis was also do to decrease blast/or increase clast levels also and a disruption in osteoid?

Yea true. I guess what I was trying to say is that there in increased bone resorption in CRI because the bone is trying to buffer the increased anion gap metabolic acidosis by releasing the calcium OHy appetite. And then as you stated, there is decreased mineralization, essentially due to the same reasoning (metabolic acidosis), so I guess that is what accounts for both osteomalacia and osteoporosis.

 

[Ramoray]

Yea, actually (I learnt this on my IM rotation) you don't end up going on dialysis until your cr. cl is wayy high--like >10 or so, I think (I forgot the real #). But, I mean eventually you will end up on dialysiss with CRI. But, anyways this is irrelevent. And, yea Iron can do it too




Yea true. I guess what I was trying to say is that there in increased bone resorption in CRI because the bone is trying to buffer the increased anion gap metabolic acidosis by releasing the calcium OHy appetite. And then as you stated, there is decreased mineralization, essentially due to the same reasoning (metabolic acidosis), so I guess that is what accounts for both osteomalacia and osteoporosis.

Hidden, here is my understanding of the whole process. So there are 2 groups of changes that happen like everyone was reffering to.
1. Low turnover problems like Osteomalacia, like we explained problems in minteralization but no turnover of the ostoid

2. High turnover problems- Osteitis fibrosa cystica with Osteosclerosis and Osteoporosis. In the early stages when PTH initially is high that acitivates Clasts via blasts with RANKL etc. and you have highly increased clast activity. At first, just like in early stages of osteoporosis(assuming its high turnover type of osteoporosis and not lowturnover type of aging with loss of blasts), you have compensatory increased blast activity to try to keep up, resulting in increased laying down of woven cortical bone and high turnover. At this poinht this is Von Renkl or ost fib cystica, where there is the brown tumor and no real loss of the amount of bone but rather it is weak woven bone layed down in high amounts in the cortex.
As the disease progresses, just as in osteoporosis(high turnover type) after awhile the blasts are not able to keep up and the Clast activity predominates leading to a spiral downhill of breakdown of bone osteoid and mass with no compensatory blast laying down woven or anything therefore you get the decreased bone density which is Osteoporosis. So i believe it happens in a timeline fashion, once blasts cant keep up Ost Fibrosa cystica signs subside and are dominated by the decreased bone density of osteoporosis.

 

[dcpark74]

sorry everyone,

i think school is getting to me...final exams. 😳

my bad.

 

[HiddenTruth]

Hidden, here is my understanding of the whole process. So there are 2 groups of changes that happen like everyone was reffering to.
1. Low turnover problems like Osteomalacia, like we explained problems in minteralization but no turnover of the ostoid

2. High turnover problems- Osteitis fibrosa cystica with Osteosclerosis and Osteoporosis. In the early stages when PTH initially is high that acitivates Clasts via blasts with RANKL etc. and you have highly increased clast activity. At first, just like in early stages of osteoporosis(assuming its high turnover type of osteoporosis and not lowturnover type of aging with loss of blasts), you have compensatory increased blast activity to try to keep up, resulting in increased laying down of woven cortical bone and high turnover. At this poinht this is Von Renkl or ost fib cystica, where there is the brown tumor and no real loss of the amount of bone but rather it is weak woven bone layed down in high amounts in the cortex.
As the disease progresses, just as in osteoporosis(high turnover type) after awhile the blasts are not able to keep up and the Clast activity predominates leading to a spiral downhill of breakdown of bone osteoid and mass with no compensatory blast laying down woven or anything therefore you get the decreased bone density which is Osteoporosis. So i believe it happens in a timeline fashion, once blasts cant keep up Ost Fibrosa cystica signs subside and are dominated by the decreased bone density of osteoporosis.

o ok, great, thanks for the explanation on the integrated process. I definately did not think of it as a timeline fashion and linked the two processes together. The postmenopausal osteoporsis mechanism is pretty much the same as that induced by hyperparathyroidism (both activating osteoclasts, leading to their respective disease processes), maybe to different extents of osteoclast activation, who knows. And, I know that you don't actually get the postmenopausal op full blown 'till at least after a decade or so, because the OB are trying to keep up. So, then it would be valid to assume that both those processes (hyperPTH induced OC activ, and estrogen deficient activ of OC), have very similar mechanisms, and the reason you see Osteit. fibrosa cyst in one, and perhaps not the other, is likely due to the extent of the OC activ?, or am i missing any other concept here? Does that make sense? I understand that the hyperPTH induced OC activ wll eventually become osteoporosis too, according to what you said. Just trying to put things together.

Aside from what you said, I also think metabolic acidosis in CRI, over time, is a pretty strong stimulus for bone resorption to buffer the acidosis, eventually leading to osteoporosis. Our friend, goljan mentions that. Robbins gooes to talk about that, but doesn't explicitly say that it causes osteoporosis, but it makes sense (high turnover). I don't know--

 

[HiddenTruth]

sorry everyone,

i think school is getting to me...final exams. 😳

my bad.

aww, such a kodak moment. Everyone apologized and made up, and now we're one big happy family again. 😀

(Alrite, i'm really not gay--just a friendly disclosure) 🙂

 

[HiddenTruth]

bizzump for pox

 

[bumblebee29]

What's the difference between a brown tumor and osteitis fibrosa cystica? I read somewhere that central degradation of brown tumor produces severe diffuse osteoclastic resorption, cystic lesions and fibrous marrow replacement. Does this mean that OFC is a sequela of brown tumor?