Review of Preclinical and Clinical Studies Supporting the Role of Polydeoxyribonucleotide in the Treatment of Tendon Disorders

Abstract

Tendon disorders are among the most common musculoskeletal conditions, accounting for 30% to 50% of all sports-related injuries. Injured tendons heal slowly and often fail to regain their original structural integrity and mechanical strength, creating significant challenges for physicians. Recently, investigations have reported that polydeoxyribonucleotide (PDRN) plays a key role in promoting tendon healing. For example, preclinical studies indicate that PDRN can enhance tendon repair by inhibiting inflammation and cell apoptosis while promoting collagen production. In clinical studies, the effectiveness and safety of PDRN were also confirmed for managing several conditions, including plantar fasciitis, epicondylitis, Achilles tendinopathy, pes anserine tendinopathy, and chronic rotator cuff disease. In light of these findings, this article aims to review the preclinical and clinical studies that support the role of PDRN in the treatment of tendon disorders. A search was conducted in Medline and PubMed from January 1994 to October 2024 to find relevant research. Ultimately, the review included 3 preclinical studies and 8 clinical studies, involving a total of 318 patients. In conclusion, PDRN is a promising therapeutic option for treating tendon disorders. However, further preclinical and clinical studies are needed to better understand its effects on tendon disorders and to support future clinical applications.

Figure 1

Schematic diagram summarizing the basis of polydeoxyribonucleotide (PDRN) efforts: the healing-promoting effect of PDRN appears to be mediated by the activation of adenosine A2A receptor or the “salvage pathway”. Following tissue injuries, PDRN activates the adenosine A2A receptor, facilitating a more complete tissue regeneration process. On the other hand, it stimulates the salvage pathway to enhance DNA synthesis and repair, resulting in faster tissue regeneration. DNA – deoxyribonucleic acid; DNase – deoxyribonuclease. Created with Adobe Photoshop software version 26.2.

Figure 2

Schematic diagram summarizing the roles and mechanisms of polydeoxyribonucleotide (PDRN) in the treatment of tendon disorders based on preclinical investigations. PDRN inhibits inflammation by decreasing the expression of the pro-inflammatory cytokines, including TNF-α and IL-6, thereby enhancing tendon repair. PDRN suppresses cell apoptosis by reducing the expression of caspase-9/3 and Bax while increasing Bcl-2 expression, thereby promoting tendon healing. PDRN encourages type I collagen synthesis by enhancing the expression of TGF-β1, VEGF, and FGF, thereby improving tendon healing. PDRN – polydeoxyribonucleotide; ↑ – increase; ↓ – decrease; TNF-α – tumor necrosis factor alpha; IL-6 – interleukin 6; TGF-β1 – transforming growth factor-beta 1; VEGF – vascular endothelial growth factor; FGF – fibroblast growth factor. Created with Adobe Photoshop software version 26.2.