Post-traumatic arthritis: overview on pathogenic mechanisms and role of inflammation

Abstract

Post-traumatic arthritis (PTA) develops after an acute direct trauma to the joints. PTA causes about 12% of all osteoarthritis cases, and a history of physical trauma may also be found in patients with chronic inflammatory arthritis. Symptoms include swelling, synovial effusion, pain and sometimes intra-articular bleeding. Usually, PTA recoveries spontaneously, but the persistence of symptoms after 6 months may be considered pathological and so-called chronic PTA. A variety of molecular, mechanobiological and cellular events involved in the pathogenesis and the progression of PTA have been identified. The activation of inflammatory mechanisms during the PTA acute phase appears to play a critical role in the chronic disease onset. Human studies and experimental models have revealed that a series of inflammatory mediators are released in synovial fluid immediately after the joint trauma. These molecules have been proposed as markers of disease and as a potential target for the development of specific and preventative interventions. Currently, chronic PTA cannot be prevented, although a large number of agents have been tested in preclinical studies. Given the relevance of inflammatory reaction, anticytokines therapy, in particular the inhibition of interleukin 1 (IL-1), seems to be the most promising strategy. At the present time, intra-articular injection of IL-1 receptor antagonist is the only anticytokine approach that has been used in a human study of PTA. Despite the fact that knowledge in this area has increased in the past years, the identification of more specific disease markers and new therapeutic opportunities are needed.

Maximum shear strain-based algorithm can predict proteoglycan loss in damaged articular cartilage

“…This load-dependent FCD loss is consistent with an earlier experimental study where the amount of dead cells increased with peak compressive load (Fehrenbacher et al 2003), which may lead to a decrease in the local FCD due to decreased synthesis. Furthermore, when the two commonly observed changes in PTOA [i.e., reduced collagen fibril integrity (Punzi et al 2016) and increased tissue permeability (Sauerland et al 2003)] were tested, the FCD loss was increased in both cases, as expected. Similar changes in tissue properties and decrease in GAG coverage (associated with FCD loss) have been observed in experimental models of PTOA (Fischenich et al 2017).…”

Routine X‐rays for suspected frozen shoulder offer little over diagnosis based on history and clinical examination alone

“…The majority of these patients were in an age group for which there might be a suspicion of moderate to severe OA (72–92‐year age group); two patients were younger (56 and 59 years of age, respectively). There is evidence to suggest that OA can present at an earlier age following joint trauma (Punzi et al, ). Both of the younger patients in the present study also had a previous history of trauma to their shoulder, so it would be expected that they would have more severe osteoarthritic changes.…”

Lower extremity osteoarthritis: optimising musculoskeletal health is a growing global concern: a narrative review

“…Following joint trauma, 20%–50% of people develop OA (around 12% of all OA cases) 31. Injury surveillance within the general population is challenging, and available data only hint at true injury rates.…”