No abstract

Background: Insertional Achilles tendinopathy (IAT) is characterized by tendon degeneration and thickening near the tendon-bone insertion.11 Calcaneal impingement is believed to contribute to the pathogenesis of IAT.5 However, it is unclear how increased tendon thickness in individuals with IAT influences impingement. This study aimed to compare Achilles tendon impingement in individuals with and without IAT. Methods: Eight healthy adults and 12 adults with clinically diagnosed symptomatic IAT performed a passive flexion exercise during which ankle flexion angle, anterior-posterior (A-P) thickness, and an ultrasonographic image sequence of the Achilles tendon insertion were acquired. The angle of ankle plantarflexion at which the calcaneus first impinges the Achilles tendon, defined as the impingement onset angle, was identified by (1) a anonymized observer (visual inspection method) and (2) a computational image deformation-based approach (curvature method). Results: Although the 2 methods provided different impingement onset angles, the measurements were strongly correlated ( R2 = 0.751, P < .05). The impingement onset angle and the thickness of the Achilles tendon insertion were greater in subjects with clinically diagnosed IAT ( P = .0048, P = .0047). Furthermore, impingement onset angle proved to have a moderate correlation with anterior-posterior thickness ( R2 = 0.454, P < .05). Conclusion: Our findings demonstrated that increased tendon thickness in IAT patients is associated with larger impingement onset angles, raising the range of ankle angles over which the tendon is exposed to impingement. Clinical Relevance: Increased susceptibility to impingement may exacerbate or perpetuate the pathology, highlighting the need for clinical strategies to reduce impingement in IAT patients.

While most mammalian tissue regeneration is limited, the Murphy Roths Large (MRL/MpJ) mouse has been identified to regenerate several tissues, including tendon. Recent studies have indicated that this regenerative response is innate to the tendon tissue and not reliant on a systemic inflammatory response. Therefore, we hypothesized that MRL/MpJ mice may also exhibit a more robust homeostatic regulation of tendon structure in response to mechanical loading. To assess this, MRL/MpJ and C57BL/6J flexor digitorum longus tendon explants were subjected to stress‐deprived conditions in vitro for up to 14 days. Explant tendon health (metabolism, biosynthesis, and composition), matrix metalloproteinase (MMP) activity, gene expression, and tendon biomechanics were assessed periodically. We found a more robust response to the loss of mechanical stimulus in the MRL/MpJ tendon explants, exhibiting an increase in collagen production and MMP activity consistent with previous in vivo studies. This greater collagen turnover was preceded by an early expression of small leucine‐rich proteoglycans and proteoglycan‐degrading MMP‐3, promoting efficient regulation and organization of newly synthesized collagen and allowing for more efficient overall turnover in MRL/MpJ tendons. Therefore, mechanisms of MRL/MpJ matrix homeostasis may be fundamentally different from that of B6 tendons and may indicate better recovery from mechanical microdamage in MRL/MpJ tendons. We demonstrate here the utility of the MRL/MpJ model in elucidating mechanisms of efficient matrix turnover and its potential to shed light on new targets for more effective treatments for degenerative matrix changes brought about by injury, disease, or aging.