Concerns regarding Palee et al. and reasserting the underlying mechanism of action in percutaneous tenotomy

Dear Editor,

We read with interest the recent article by Palee et al., “Tendon modification with percutaneous Ultrasound-Guided Tenotomy using TENEX®,” in Interventional Pain Medicine. The authors presented a detailed ex vivo analysis of the macroscopic and histologic changes in a bovine cadaveric model exposed to the Tenex tenotomy device; however, we believe several key biologic and clinical considerations were overlooked that could mislead readers about the established mechanism of tenotomy procedures.

The clinical relevance of paratenon separation in a healthy bovine tendon model is unclear, particularly since the paratenon was removed during the tissue preparation:

“[t]he Achilles tendon samples were resected … followed by the removal of the fascia and paratenon of the Achilles.”

This confounds the interpretation of histologic findings, especially in biologically inert cadaveric tissue. The authors use the terms “paratenon” and “peritendinous tissue” interchangeably when describing post-procedural changes, adding to the confusion. This study also did not account for the pathologic features of tendinopathy, including collagen disarray, increased ground substance in the extracellular matrix, and mucoid degeneration [1].

Substantial clinical and preclinical evidence suggests that the therapeutic effect of tenotomy procedures—whether performed with a scalpel, needle, or the Tenex device—stems from initiating a biologically-mediated healing response rather than paratenon disruption alone. Preclinical and imaging studies have shown that tenotomy procedures trigger a healing cascade by stimulating bleeding, clot formation, angiogenesis, and recruiting reparative tenocytes [2,3]. Tenotomy procedures using the Tenex device have been shown to not only remove pathologic tissue [2], but also restore tendon structure and function [3]. Thus, tenotomy's efficacy lies in stimulating a targeted healing response, not disruption disrupting the paratenon.

Complete disruption of the paratenon may be counterproductive, particularly in the absence of paratenon dysfunction. Therefore, we respectfully disagree with the clinical recommendation by Palee et al. to achieve paratenon separation as a means to alleviate chronic tendon pain. While there is likely no current consensus regarding the optimal technique, we are not aware of any clear, objective measurement or peer-reviewed scale that the authors used to base their assessments. Instead, we recommend a more widely accepted procedural endpoint—the debridement of pathologic tissue until palpable changes in tissue texture [4].

While we recognize that the paratenon is a potential pain generator and a therapeutic target in Achilles or patellar tendon pathology [5], this mechanism proposed by Palee et al. would not explain the successful treatment of the rotator cuff, plantar fascia, or common extensor tendon with this technology, which all lack a paratenon [6]. The paratenon also appears to play a vital role in tendon homeostasis [7], and a crucial role in tendon healing by supporting neovascularization and cellular proliferation [8]. Clinically, paratenon-preserving techniques have been associated with lower complication rates and improved outcomes in Achilles tendon surgery [9].

Lastly, the technique description does not reflect the standard of care and is insufficient for replication in vivo. The “oscillatory” description does not clarify whether the device was moved slightly without passing through tissue, or whether it was passed back and forth through the cadaveric tissue. In addition, ultrasound-guidance was not utilized, and it's unclear the zone of tissue affected beyond the MicroTip and how close the device tip came to the “control.”

1. Conclusion

The emphasis of Palee et al. on the paratenon, penetration depth of the device, and cutting times, although valuable from an engineering perspective, ignores the core biological process of healing. The omission of the inflammatory and remodeling cascade in Palee et al.’s mechanistic interpretation of these procedures is a notable oversight, one that should be addressed to ensure clarity for both clinicians and researchers.

Declaration of competing interest

The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Walter I. Sussman reports a relationship with Trice Medical that includes: consulting or advisory. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.