## 1 Introduction  
Peripheral neural interfaces are high tech devices able to record neural signals and evoke neural activity through the stimulation of axonal clusters. Different types of intra-neural electrodes have been designed [1, 2, 3, 4] to be directly inserted within peripheral nerves or to be implanted through micromet needles [5, 6, 7], while other types of regenerative neural interfaces were studied [1, 8, 9] to exploit the axonal regeneration [10, 11, 12, 13]. In particular, intranearal interfaces were able to provide selective recording and stimulation, keeping their overall invasiveness low. Unfortunately, as the foreign body reaction (FBR) affects the interaction between living tissue and synthetic materials [14, 15], similarly it affects the interaction between the peripheral nervous tissue [16, 17, 18, 19, 20, 21, 22, 23] and intranearal interfaces [24, 25, 26], resulting in the formation of a tissue capsule [27, 28] around the implanted structures. Several studies explored the FBR details describing a first phase related to the adsorption of blood and plasma proteins (e.g., fibrinogen, fibronectin, albumin and antibodies) to the implant surface [29, 30]. Therefore, a second phase was described where the adsorbedprotein layer promoted monocyte and leukocyte extravasation, attraction and adhesion to the surface, together with the coagulation cascade [31; 32; 33]. Then, a sort of matrix of fibrin was found to attract circulating leukocytes and local macrophages around the surface of the implanted material under the chemical attraction of chemokines [32; 34]. Furthermore, it was described as the way extravasated monocytes differentiate to macrophages and fuse together to form multinucleated foreign body giant cells (FBGCs). These cells started releasing further inflammatory cytokines, boosting the inflammatory response through a positive feedback mechanism [35; 36]. Then, it was described as myofibblasts triggered a massive secretion of extracellular matrix (ECM) components [15; 27; 37]. Finally, at the end of the whole process, the scar tissue capsule was found to be impermeable to the nonspecific immune system and to many chemicals [14; 15; 27]. Both the complexity of the FBR [14; 15; 27; 28; 29; 30; 31; 32; 33; 34; 35; 36; 37; 38] and the unclear relationship between the physical properties of peripheral nerves [7; 39; 40; 41; 42; 43; 44; 45; 46; 47; 48] and the amount of scar tissue production makes a reliable prediction of the capsule thickness a challenging task. Some previous studies explored the evolution of the FBR caused by intraneural electrodes longitudinally implanted (e.g., LIFE electrodes [49; 50]) in the rat peripheral nerves, while others explored the cellular composition and the thickness of the fibrotic capsule in a time span ranging from 1 day to 8 months [51; 52]. These investigations revealed that the contacts between the nerve fibers and the electrode active sites were partially lost because of the outgrowth of the encapsulating tissue. In particular, the increase of the scar capsule was directly related to the increase of the electrical impedance, resulting first in the decrease of the signal to noise ratio [53] and possibly in a sensible drop of registration and stimulation capabilities [36; 54]. Therefore, a correct and quantitative assessment of the capsule thickness over time is crucial information to improve the design of intraneural interfaces as well as their implantation technique. However, the development of the FBR involves several interrelated complex processes [14; 15; 27; 28; 29; 30; 31; 32; 33; 34; 35; 36; 37; 38] which are partially hidden since their explicit and physically based rules are not known in all details. Nevertheless, it is a pressing issue to investigate whether computational strategies are able to reproduce the scar tissue evolution, making sense of the huge complexity of the underlying phenomena. In particular, a suitable trade off between light computational models and physically meaningful dynamics has to be found.