Following on from yesterday’s posts on Osteoporosis (OP), I thought I’d explore the basic science behind a cause of it we rheumatologists are particularly interested in: OP secondary to chronic inflammation.
But I struggled, hence the late post. I struggled scientifically to understand the still murky science of Osteoimmunology. I struggled philosophically to make sense of what survival or defence advantage OP would confer on the immune system trying to fend off enemies (like germs & cancer), even if it may be misguided sometimes to cause autoimmunity. I can understand anaemia and cachexia, but not OP. Not yet, anyway. Anyone care to enlighten me?
Borrowing from IBD research, an organ pretty much far removed from bone compared to arthritis, this paper tries to elucidate the link between chronic inflammation and OP.
The picture I’m getting in struggling through this and the previous article, seems to me like the bone marrow is some sort of war room, where competing (or counter-balancing) immune teams carve out survival niches to hunker down for the long haul and do their horse-trading, far removed from the heat of the battle (eg the gut, in IBD’s case). The bone breakers (osteoclasts) and builders (osteoblasts) are mere workers remodeling the teams’ bunkers. Depending on which team has the upper hand in the protracted course of a chronic disease, we may see mainly OP predominate in a particular phase, or new bone formation (eg osteophytes, syndesmophytes) in another, as in AS and PsA. Or, as we’ll see in tomorrow’s post, both processes happening at the same time in separate compartments, as in OA.
Of course, this may be far from the truth, but this is how I make sense of my complicated immune world for now.