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Low Back Pain and Disability

Did you know that low back pain causes more disability than any other condition globally? As such, the development, or ‘pathogenesis’, of low back pain has long been investigated by research groups and programs. Most recently, the esteemed Drs. Injeyan, Injeyan, and Triano compared differences in inflammatory markers in the blood between asymptomatic individuals, and patients with non-specific acute or chronic low back pain. While there are limitations to every study, their results highlighted a distinct increase in pro-inflammatory mediators and a marked decrease in anti-inflammatory mediators in both groups of symptomatic patients when compared to asymptomatic individuals. Interestingly, a separate group in 2016 looked at the various effects of spinal manipulation and found that this technique may in fact activate naturally-produced anti-inflammatory mediators.

Inflammation and OA

Osteoarthritis (OA) was previously considered non-inflammatory. It is now well recognized that inflammatory mediators are produced and can be measured in joint fluids of patients with OA. This inflammation is a major risk factor in cartilage loss, pain, swelling, and stiffness. When management and treatment of OA consists of anti-inflammatory components, patients can improve their function and decrease pain levels. Platelet-rich plasma (PRP) is a cell therapy, that uses one’s own blood through joint injections, to reduce inflammation. Platelets are a high source of concentrated growth factors and inflammatory mediators. Platelets in PRP release many types of anti-inflammatory proteins that signal cells that lead to suppression of inflammation in OA.

 

Goldring and Otero. Inflammation in Osteoarthritis. Curr Opin Rheumatol. 2011; 23

Xie et al. Biology of platelet-rich plasma and its clinical application in cartilage repair. Arthritis Res Ther. 2014; 16