## 1 Introduction  
Acute injuries of the tendons are among the most common in the human body [1]. The injured tendon healing process consists of three main phases, which are essential for soft tissue healing. However, in the case of an incomplete healing process, degeneration of the tissue may occur [2]. The tendinopathy process is characterized by the uncontrolled production of both collagenous and non-collagenous extracellular matrix (ECM), apoptosis in the local fibroblast population, and chaotic invasion of newly formed capillaries [2; 3; 4; 5; 6; 7; 8]. These histopathological alterations are reflected in decreased mechanical durability of the tendon and clinically manifest as tendinopathy. The healing of the injured tendon is conducted by a complex network of cytokines and mediators, which dynamically interact during regeneration of the tendinous tissue. This can be used in the therapy of tendon disorders [2; 9]. The presence of specific types of growth factors in adequate time is crucial to fully recovering the tissue [2; 9; 10; 11]. Many agents, such as mesenchymal stem cells (MSCs), growth factors, and hemostatic agents, have been studied to improve the tendon healing process [4; 12; 13; 14; 15]. It is currently believed that five main growth factors play a crucial role in the tendon healing process: insulin-like growth factor-1 (IGF-1), transforming growth factor-\(\beta\) (TGF-\(\beta\)), vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and basic fibroblast growth factor (bFGF). Further, all of them are included in platelet-rich plasma (PRP). This is an autologous plasma fraction with a platelet-rich cellular component containing growth factors in alpha granules [16]. The efficacy of platelet concentrates in promoting wound healing and tissue regeneration is at the center of a recent academic debate [17]. Some authors even tried this therapy in osteonecrosis; however, the results are not sufficient to establish this method as a gold standard [18]. Moreover, the regeneration process demands cells to supply the local fibroblast population responsible for extracellular matrix production [2]. Recent studies revealed the positive role of MSCs, which are the progenitors for the fibroblast population, in tendon injury therapy [19; 20; 21]. Moreover, [PERSON] et al. suggested that autologous microfragmented adipose tissue reduces the inflammatory and catabolic markers in tenocytes [22]. Other authors isolated the extracellular vesicles from human adipose-derived MSCs to develop new therapeutic approaches in osteoarthritis [23]. The most common and well-established system to quantify the pathological changes in tendinous tissue is the Bonar scale [24; 25]. The Bonar scoring system is based on four main variables: tenocyte morphology, ground substance accumulation, the extent of the neovascularization process, and the disruption of the collagen bundle architecture. Each variable is assessed on the scale of 0 to 3 points, where 0 indicates a normal appearance of tendinous tissue and 3 indicates the most severe detectable pathology [24]. The Bonar scoring system serves in the microscopic evaluation of the various regions of tendon pathology, but on the other side, it can be easily used reversely to investigate the decreasing degeneration after effective treatment and quantify the healing progress [24; 26; 27; 28; 29; 30]. The link between the histopathological scale and therapeutic advances of various treatment methods in chronic tendon disorders has been evaluated in only a few studies. Despite the numerous reports about improved clinical conditions after tendon treatment based on functional scales, surprisingly, the microscopic state of the tissue was not assessed [31; 32]. We believe that there is a real need for a connection between clinical observations and tissue alterations arising during the treatment, to gain superior functional outcomes.