INTRODUCTION: Peritoneal adhesions are pathological fibrotic connections forming between organ surfaces. They typically develop following a surgical procedure of the thorax, abdomen or pelvis, or result from inflammatory diseases. Peritoneal adhesions can cause small bowel obstruction, chronic pain or infertility and are identified nowadays as a major economic and health burden. However, the underlying mechanisms of tissue physiological repair and adhesion formation are still poorly understood [1]. The role of biomechanics is critical to provide better understanding, prevention and treatments for peritoneal adhesions, especially regarding pain management. Indeed, nociception and mechanics are strongly connected [2]. We present a novel model of peritoneal adhesions depicting the main biochemical mechanisms associated with adhesion formation and their mechanical consequences. METHODS: We propose here a 2D model of adhesion formation representing the volume between the peritoneal membrane and the tissue boundary, where the following mechanisms occur: (i) the formation of the fibrin exudate upon tissue insult, (ii) fibroblast-mediated fibrosis and (iii) cyclic loading simulating typical breathing boundary conditions. In particular, we investigate here the evolution of main biochemical agents responsible for material properties of the medium following trauma: fibrin - the principal element in the clot formation during peritoneal wound healing; tissue plasminogen activator (tPA) - a potent coagulation agent; fibroblasts - responsible for fibrosis and membrane regeneration; collagen, the main structural element of adhesions. We implemented a system of partial differential equations depicting the time- and space- dependent evolution of fibrin, tPA and fibroblast concentrations, accounting for fibrin-mediated chemotaxis of fibroblasts in the peritoneal fluid. Additionally, the evolution of collagen content was derived from fibroblasts activity and collagen degradation. In order to simulate mechanical solicitations of the breathing cycle, we imposed a cyclic displacement of the injured serous membrane. RESULTS: In the case of a healthy repair, the inhibition of fibrin by tPA-mediated fibrinolysis prevents formation of the dense connective tissue, thus preserving the mechanical behaviour of the system. Instead, with low tPA local production, the fibrin clot develops into a dense collagenous gel binding to the neighboring membrane. As expected, this induces larger strains within the injured and the healthy tissue. DISCUSSION & CONCLUSIONS: This is the first attempt to quantify the mechanisms of adhesion formation. We successfully depicted the main events following tissue trauma. Future work will investigate the next remodelling steps, in particular involving innervation and in vivo mechanical stimulation. ACKNOWLEDGEMENTS: REFERENCES:1. Hassanabad et al., Biomed; 9(8):867 (2021). 2. Feng et al., J Neur Trans; 127(4):415–429 (2008).