“inflammation is now understood to be a key mediator of OA that contributes to cartilage loss and progressive degeneration of affected joints… OA is no longer considered a noninflammatory arthritis or a ‘wear and tear’ disease”
I heretofore thought age-related cartilage loss was the cause of osteoarthritis and inflammation. Turns out it’s the other way around: the inflammation degrades cartilage. Okay, no more slogging through joint pains for me, regardless of how small.
Edit: added a phrase for clarity



This is a field I study. Its more complicated than yes/no. OA is caused by inflammation. However, inflammation when introduced into a joint space raises the friction coefficient between surfaces within the joint. More friction leads to mechanical stress and deterioration.
The friction coefficient for synovial joints ranges from 0.0015 - 0.01 depending on the study. Essentially frictionless. That’s why when inflammation enters the synovial fluid, you hear crepitus or “creaking”. Friction goes up and tendons vibrate like strings on a violin. For reference, ice on a Teflon pan has a friction coefficient of 0.05 - 0.10. Roughly ×5 the conservative estimate for synovial joints.
So when people told me as a kid not to worry about my crepitus, they were in fact completely wrong? If so, I’m feeling vindicated but also sore, but that’s better than only sore.
Well, I guess it depends entirely on what you could do about it. If the crepitus was brought about by chronic malmechanics then yes. If it was hereditarily driven then there’s nothing you could do about it. Typically, I preach to my patients that popping, clicking, snapping, etc. are only notable if they induce pain or if they were brought about by a change in activity.
A secondary note on pain is that it’s part of the human condition. Pain is relative and inevitable. If you live your life in a bubble then a sprained ankle is going to feel like a gunshot wound. There will always be some form pain or soreness. The trick is to address it as it comes about and shift it to the next weakest link in the chain. If you have low back pain, strengthen your core to treat it. Then that pain may shift to your hips where you have overactive or weak abductors, then it may be your neck. Who knows. But there’s few things as debilitating as chronic pain in one location. The more painful it gets, the less you’ll want to use it and you end up building a positive feedback loop.
Fair. In my case I wish someone had not overlooked the systemic inflammation (from a different condition that has been recently correlated with OA, somewhat unexpectedly) and the malmechanics I was experiencing, so that I might have avoided some of the further issues, but, so it goes.
I manage to shift some of the chronic pain, but sadly society really likes to build worlds that have only one blessed way of doing certain things, which makes it impossible to shift more consistently. So I will have to mostly content myself with smugly sore.
Given you appear to be a doctor though, I do have one favor to ask. If you ever get a flexible kid with crepitus come through your doors, maybe add a CRP test to their blood work, just on the off-chance and even if only for the chain of evidence.
Had the chance to do cadaver dissections and synovial fluid is some fascinating stuff! Slightly mucusy, but incredibly slick
Fascinating!!!