While weight loss through whatever means might have helped knee OA patients symptomatically (from other studies, not this radiological one), weight loss through exercise alone made no difference to slowing the cartilage degeneration compared to losing no weight at all).
Weight loss through diet, with or without exercise, was what it took to slow disease progression.
Structurally speaking, just diet and don't sweat it. Truth be told, for now at least.
Streptococcus appeared to be associated with more pain and worse knee OA, independent of body mass index.
Most knee pain relief occurred in the first month post-surgery, correlating with the drastic drop in leptin, a pro-inflammatory adipokine (produced by fat cell). This occurs well before any significant weight loss has even started.
Weight loss declined steadily in the first year before levelling off, corresponding to the rate of reduction of other pro-inflammatory cytokines like IL6 and IL1RA.
While it is known that fat cells enumerate pro-inflammatory adipokines which in turn drive pro-inflammatory cytokines; leptin may, in particular, drive knee OA pain. And something altered in the gastrointestinal tract by bariatric surgery (mainly bypass and sleeve gastrectomy), rather than weight loss, is responsible for this precipitous leptin crash. Alternations in the microbiome is suspect here.