OA vs. RA and Dystrophic vs. Metastatic Calcification

[MudPhud20XX]

So in OA there is no inflammation whereas in RA there is right? So why do we still use NSAIDs for OA?

So Ca2+ and phosphate ion are used to differentiate dystrophic vs. metastatic calcification. Why phosphate? Why does it correlate with Ca2+?

Many thanks in advance.

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[stepone2015]

OA gets NSAIDs for pain.

Metastatic calcification is caused by very high calcium levels in the blood. Calcium needs something to bind to, so it binds with the phosphate and into the tissues. Dystrophic calcification is primarily due to cellular damage of some type. Cells die and release proteins and junk, which is perfect for binding calcium. No phosphates needed.

This is me thinking it through and I may be completely wrong.

 

[MudPhud20XX]

alright thanks. so no inflammation from OA but there is pain which makes sense, but w/o inflammation why would you get pain? if the pain is due to non-inflammatory cause, why would NSAID help the pain in OA?

 

[Transposony]

So in OA there is no inflammation whereas in RA there is right? So why do we still use NSAIDs for OA?

OA is no longer considered a degenerative disease as inflammatory cytokines like IL-17 are found in the joint aspirate.
Few years ago it was considered a degenerative disease and therefore acetaminophen was the DOC.
Although acetaminophen is still recommended for mild to moderate OA, NSAIDs are recommended depending on severity & side effect profile for that particular patient.
Topical NSAIDs are preferred over oral.

 

[sloop]

If there is no inflammation in OA, that's news to me. Certainly OA doesn't have the sort of chronic inflammation/lymphocytic infiltration/pannus formation/joint swelling that you see pathologically in RA, but are people really saying there is no inflammation?

 

[MudPhud20XX]

OA is no longer considered a degenerative disease as inflammatory cytokines like IL-17 are found in the joint aspirate.
Few years ago it was considered a degenerative disease and therefore acetaminophen was the DOC.
Although acetaminophen is still recommended for mild to moderate OA, NSAIDs are recommended depending on severity & side effect profile for that particular patient.
Topical NSAIDs are preferred over oral.

alright so OA is an inflammatory dz now. thanks Transposony!

 

[sloop]

if the pain is due to non-inflammatory cause, why would NSAID help the pain in OA?

If there is no inflammation, NSAIDs will not help. I'm fairly certain that's the rule. For similar reasons, they don't lower body temperature unless there's a fever of inflammatory etiology.

 

[MudPhud20XX]

If there is no inflammation in OA, that's news to me. Certainly OA doesn't have the sort of chronic inflammation/lymphocytic infiltration/pannus formation/joint swelling that you see pathologically in RA, but are people really saying there is no inflammation?

according to my kaplan note i have

 

[stepone2015]

Way I learned it was that OA was all about degenerative damage to the joint especially articular cartilage. There's inevitably some cytokines and inflammation, but it's minimal compared to an autoimmune disease like RA.

 

[Transposony]

alright so OA is an inflammatory dz now. thanks Transposony!

I wouldn't say that since inflammation is not causing OA. A better way would be to say there is associated inflammation.
Just think about it -- if there is a mechanical injury PMNs/Lymphocytes/Macrophages are bound to go there to find out what's going on and do what they do best--> Inflammation followed by attempts at healing.

 

[sloop]

Way I learned it was that OA was all about degenerative damage to the joint especially articular cartilage. There's inevitably some cytokines and inflammation, but it's minimal compared to an autoimmune disease like RA.

This sounds like a more fair representation of the diseases.

 

[pd1112]

RA: T cells initiate autoimmune response -> primary inflammation -> synovial & cartilage hell, germinal centers, etc.
OA: Intrinsic defects in cartilage + extrinsic risk factors -> cartilage injury -> secondary inflammation, minimal cells but plenty of cytokine-mediated remodeling.

 

[nds86]

OA can be either an inflammatory disease or a noninflammatory disease. If it's non-inflammatory (initial), TX with acetaminophen (APAP) and if it's inflammatory, TX with an NSIAD or COX-2 selective (as stated above topical is preferred). From labs, PE, and Hx, you know which method to follow.

RA is an inflammatory disease.