Abstract
The role of inflammation and the mechanism of tendon healing after rupture has historically been a matter of controversy. The purpose of the present study is to investigate the role of mast cells and their relation to the NMDA receptor-1 (a glutamate receptor) during healing after Achilles tendon rupture. Eight female Sprague Dawley rats had their right Achilles tendon transected. Three weeks after rupture, histological quantification of mast cell numbers and their state of degranulation was assessed by histochemistry. Co-localization of mast cell tryptase (a mast cell marker) and NMDA receptor-1 was determined by immunofluorescence. The intact left Achilles tendon was used as control. An increased number of mast cells and a higher proportion of degranulated mast cells were found in the healing Achilles tendon compared to the intact. In addition, increased co-localization of mast cell tryptase and NMDA receptor-1 was seen in the areas of myotendinous junction, mid-tendon proper and bone tendon junction of the healing versus the intact tendon. These findings introduce a possible role for mast cells in the healing phase after Achilles tendon rupture.
Highlights
The physiological mechanisms of tendon healing and pain signaling are still far from understood and the debate continues regarding the role of inflammation in healing and tendinopathy development (Abate et al 2009; Millar et al 2017)
Intact tendons exhibited normal tissue morphology in the tendon proper, paratenon and other regions of the tendon, i.e., a normal and organized collagen structure was seen, tenocytes were tightly packed between the collagen bundles and no hyper-cellularity or evidence of vascular changes were found in the intact tissue (Fig. 1a–d)
We explored a novel aspect of mast cells (MCs): their possible involvement in tendon healing in the context of Achilles tendon (AT) rupture
Summary
The physiological mechanisms of tendon healing and pain signaling are still far from understood and the debate continues regarding the role of inflammation in healing and tendinopathy development (Abate et al 2009; Millar et al 2017). The peripheral nerve system (PNS) exhibits a key role in regulating inflammation, pain signaling and healing of the damaged tissue via afferent to efferent pathways (Chiu et al 2012). Peripheral nerve endings at the site of injury can emit potent neuromediators with the ability to modify the function of fibroblast-like cells in the healing tendon tissue (Ackermann et al 2014; Murphy and Hart 1993). Emitted neuronal substances may interact with resident mast cells (MCs) and macrophages to affect their function (Chiu et al 2012; Murphy and Hart 1993). MCs contain substances that, when emitted, may alter the function of both the PNS and tissue cells (Hart et al 1998). It has been hypothesized that MCs residing near nerve endings may degranulate and affect the
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