Sympathetic Innervation and Adrenergic Receptors in Equine Deep Digital Flexor Tendinopathy: Preliminary Results

• Published in: Journal of comparative pathology 2018-08, Vol.163, p.33-37
• Main Authors: Beccati, F., Pepe, M., Antinori, L., Pascucci, L., Chiaradia, E., Mandara, M.T.
• Format: Article
• Language: English
• Subjects: Animals; equine deep digital flexor tendinopathy; Horse Diseases - metabolism; Horse Diseases - physiopathology; Horses; Receptors, Adrenergic, alpha-1 - metabolism; sympathetic innervation; Sympathetic Nervous System - metabolism; Sympathetic Nervous System - physiopathology; Tendinopathy - metabolism; Tendinopathy - physiopathology; Tendinopathy - veterinary; Tendons - innervation; Tendons - metabolism; tyrosine hydroxylase; α-1 adrenergic receptor
• ISSN: 0021-9975; 1532-3129
• DOI: 10.1016/j.jcpa.2018.07.005

The aim of this study was to delineate the pattern of sympathetic innervation in the suprasesamoidean region of the deep digital flexor tendon (DDFT) in horses with tendinopathy by immunohistochemical labelling for tyrosine hydroxylase (TH) and α-1 adrenergic receptor (α1-AR). Twelve forelimbs were obtained from 10 horses with DDFT tendinopathy and six feet obtained from six horses were used as healthy controls. Post-mortem radiographic, ultrasonographic and gross examinations were performed on the suprasesamoidean area of the DDFT to assess the presence of tendinopathy. Longitudinal sections were collected and processed. Lesions were classified as core lesions, dorsal border lesions and parasagittal oblique splits. Immunohistochemistry was performed and the degree of immunoreaction was classified as absent, mild or marked. Seven core lesions, four dorsal border lesions and one parasagittal oblique split were identified. There was no increased expression of sympathetic innervation in samples with a dorsal border lesion of the DDFT compared with healthy samples. In contrast, core lesions showed increased expression of α1-AR and reduced expression of TH, which supports the hypothesis of a compensatory imbalance between the sympathetic mediator and the sympathetic receptors as a cause or effect of structural damage. In addition, adrenergic activation could stimulate cell proliferation and differentiation within these lesions.