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

The research involves examining the distribution of sympathetic nerves and adrenergic receptors in the region of deep digital flexor tendon (DDFT) in horses suffering from tendinopathy. It reveals that core lesions show an increase in α1-AR expression and decrease in tyrosine hydroxylase expression, suggesting an imbalance that might contribute to or result from structural damage.

Research Objective and Methodology

• The primary goal of the study was to investigate the pattern of sympathetic innervation in the region above the sesamoid bone (suprasesamoidean area) of the deep digital flexor tendon (DDFT) in horses suffering from tendinopathy.
• This investigation was carried out by labelling enzymes and receptors, specifically tyrosine hydroxylase (TH, an enzyme involved in the production of catecholamines such as adrenaline) and α-1 adrenergic receptor (α1-AR, a receptor responding to adrenaline), using immune histochemical methods.
• The study included twelve forelimbs from ten horses with DDFT tendinopathy and six healthy feet obtained from six horses as a control group.
• Post-mortem examinations using radiography, ultrasonography, and physical assessment were performed on the DDFT’s suprasesamoidean area to confirm the presence of tendinopathy.

Classifying and Evaluating Lesions

• The researchers collected and processed longitudinal sections of the affected areas and classified the lesions into three types: core lesions, dorsal border lesions, and parasagittal oblique splits.
• Immunohistochemistry was carried out on these sections and the extent of the immunoreaction was classified as either absent, mild, or marked. This gives an indication of the presence and degree of the response by the immune system in the area, showing the level of the disease’s progression.

Key Findings

• Seven core lesions, four dorsal border lesions, and one parasagittal oblique split were identified in the study.
• The study found no heightened expression of sympathetic innervation (nerve fibers related to the fight or flight response) in samples with a dorsal border lesion of the DDFT compared against healthy samples.
• On the contrary, core lesions exhibited an increased expression of α1-AR and a reduced expression of TH, which provides evidence to support the theory of a compensatory imbalance between the action of the sympathetic system (mediator, in this case, adrenaline) and the receptors of the sympathetic system (α1-AR).
• This imbalance could either be a cause or an effect of the structural damage seen in the form of core tendinopathy lesions.
• Furthermore, the study suggests that activation of the adrenergic system, responsible for the release and regulation of adrenaline, could stimulate cell proliferation and differentiation within these lesions, potentially contributing to tissue repair or the progression of the disease process.