If we are serious about preventing Osteoarthritis, we have to start treating when it can still be prevented: at the bone marrow edema stage. The only way to diagnose BME/BML is with MRI. The most cost-effective treatment may be with an anti-resorptive agent targeting the osteoclasts.
The jury is still out, but I consider OA as primarily a subchondral bone plate failure, whereby chondrogenesis (cartilage regeneration) cannot keep pace with cartilage destruction. The latter may be due to normal or accelerated wear-and-tear, through sports trauma, biomechanical overloading, or chronic inflammation. Regenerative inadequacy is genetically-weighted and part of aging.
Whatever the trigger or pro-inflammatory cytokine pathway, the common agent of bone destruction is the osteoclast.
As proof of concept, there are reports of Bisphosphonates and Denosumab helping to resolve BME/BML as well as pain.
Anecdotally, I have managed to relieve pain lasting 2-6 months in refractory knee OA patients using Zoledronic acid or Denosumab.
Larger placebo-controlled studies are needed to determine if this translates to significant reduction in the number of eventual OA cases.
If the horse has bolted and you've got radiographic OA, your aim for the rest of your life is to avoid or delay the need for joint replacement surgery.
You'll be clutching at straws trying out glucosamine/chondroitin, fish oils, avocado-soyabean, ginger/tumeric extracts, Diacerein, Strontium Ranelate, viscosupplementation, etc mainly for pain relief.
You'll be perusing articles like this: 1 year of weight management (read dieting), exercise, physical therapy and counselling just to feel and function that wee bit better.
We so need to rethink OA treatment: to OA prevention. The "early and aggressive" treatment paradigm in RA/SpA/PsA needs to be transplanted to OA.
Like BME/BML, meniscal tears are harbingers of eventual OA development and progression.
Profiling who will end up with a total knee/hip joint replacement: being OVERWEIGHT stands out.