Both conformation and equine breed contribute to the development of suspensory ligament (SL) degeneration, especially when coupled with aging and the presence of pituitary pars intermedia dysfunction (PPID).
While concentration of plasma total cortisol tends not to be elevated in PPID horses, biologically active, free unbound cortisol fractions are significantly more elevated in PPID horses than in healthy horses. These fractions are able to bind to cytoplasmic steroid receptors. In addition, about one-third of PPID horses also suffer from insulin dysregulation.
Researchers evaluated postmortem suspensory ligaments of horses with and without PPID for glucocorticoid receptors (GCR), insulin, and a host of enzymes that act on cortisol [Hofberge,r S.C.; Gauff, F.; Thaller, D.; et al. Assessment of tissue-specific cortisol activity with regard to degeneration of the suspensory ligaments in horses with pituitary pars intermedia dysfunction. AJVR vo. 79, no. 2, Feb 2018; pp. 199-210].
Twelve horses, aged 16-25 years of age with postmortem changes suggestive of PPID, were used in the study. Nine of the 12 had typical PPID clinical signs; eight of these nine also had elevated ACTH concentrations. The other three horses had no clinical signs of PPID or plasma elevated ACTH. Six other horses, aged 14-23 years, had no clinical record or postmortem signs of PPID and were used as controls along with six young non-PPID horses aged 2-9 years. Two non-PPID horses were treated with dexamethasone.
Horses with PPID had higher levels of GCRs in the SLs and greater enzyme activity in the SL and neck skin samples. The presence of glucocorticoids has known adverse effects on tendon fibroblasts, such as suppression of tenocyte activity and disturbance to proteoglycan production. Suspensory ligaments contain tenocytes so are subject to the adverse effects incurred from elevated free unbound cortisol elevations, such as reduction in tensile strength of the tissue.
Accumulation of proteoglycan is documented in horses with degenerative SL desmitis and this is significant because in these cases, water-binding proteoglycans are increased by five-fold to elicit tissue swelling and SL degeneration. The two non-PPID horses treated with dexamethasone developed high levels of GCR and enzymes comparable to those horses with PPID.
The take home message of this study concluded, “Horses with SL degeneration should be screened for PPID and horses with PPID should be screened for SL degeneration to allow timely treatment with corrective trimming or shoeing or appropriate medication.”