MiMedx Group, Inc. announced two peer-reviewed studies investigating the use of micronized dehydrated human amnion chorion membrane (mdHACM) for the treatment of debilitating conditions involving degeneration of connective tissue: osteoarthritis (OA) and tendinopathy. The first study, published in Osteoarthritis and Cartilage Open, identified a novel mechanism of action by which PURION? Processed mdHACM regulates degradative processes in human articular chondrocytes, the primary cell type comprising articular cartilage. These results further support mdHACM as an investigational new drug (IND) candidate for the treatment of OA and highlight potential disease modifying activities. The second study, published in the Journal of Biomedical Materials Research, Part B, examined chronicity and poor outcomes following tendon injury attributable to prolonged inflammation and hypervascularity. These complications were modeled in vitro for the purposes of evaluating mdHACM as a treatment for tendinopathy, which led to the identification of specific mechanisms responsible for counteracting these disease processes. With more than 300 million global cases of hip and knee OA and the current treatment paradigm focusing primarily on symptomatic relief (Non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroid injections) followed by prosthetic joint replacement when needed, developing a regenerative therapy that addresses the underlying structural damage is becoming increasingly more important. Micronized dHACM is hypothesized to target specific OA-related pathways to re-establish homeostasis, and thereby mitigate the physical effects of OA. To test this theory, an in vitro system was developed to recapitulate the disease state. OA was modeled using an established in vitro platform consisting of a 3D pellet culture of human articular chondrocytes and a cartilaginous extracellular matrix (ECM). The addition of inflammatory stimuli induced OA-like changes and elevated two key signaling pathways associated with disease progression, NF-?? (Nuclear Factor kappa-light-chain-enhancer of activated B cells) and canonical Wnt signaling. Introduction of mdHACM treatment specifically inhibited these pathways (Figure 1), effectively reversing the effects of the inflammatory stimuli and diminishing the expression and activity of key enzymes responsible for cartilage matrix degradation. While the onset of OA is likely multifactorial, this study indicates mdHACM regulation of both NF-?? and canonical Wnt signaling is one such mechanism by which this treatment elicits a chondroprotective effect and attenuates degeneration in vitro. This study substantiates previous clinical and preclinical evidence suggesting mdHACM treatment improves the outcomes associated with OA.