Beyond Overstrain: Understanding the Causes and Pathophysiology of Suspensory Ligament Injuries in Horses

Suspensory ligament (SL) injuries are among the most common musculoskeletal disorders affecting equine athletes. Despite their frequency, relatively little is known about the cellular and matrix-level changes that occur following injury. Histological studies have reported alterations in collagen fibre organisation and fibroblast viability, while ultrasonography has identified mineralisation within SL branches, although this is not always associated with clinical lameness^1,2. 

Genetic and Hereditary Influences 

Most SL injuries occur without any identifiable underlying disease or genetic abnormality. However, research has demonstrated a heritable component, particularly in Thoroughbreds, where heritability estimates range from 0.05 to 0.17¹. 

Certain inherited disorders can directly affect ligament integrity and predispose horses to injury. One such condition is Hereditary Equine Regional Dermal Asthenia (HERDA), an autosomal recessive disorder affecting Quarter Horses. Although these horses are primarily characterised by fragile, hyperextensible skin, studies have also demonstrated significantly reduced tensile strength of the superficial digital flexor tendon (SDFT), deep digital flexor tendon (DDFT), and suspensory ligament³. 

Degenerative Suspensory Ligament Desmitis (DSLD) 

Degenerative Suspensory Ligament Desmitis (DSLD), also known as Equine Systemic Proteoglycan Accumulation (ESPA), is a progressive disease with an estimated heritability of 0.22⁴. Affected horses often develop bilateral or quadrilateral lameness that does not improve with rest. 

The condition is characterised by collagen fibre disorganisation and excessive accumulation of proteoglycans within the ligament and other connective tissues. Studies have reported elevated levels of aggrecan, aggrecanases such as ADAMTS4 and ADAMTS5, and inter-alpha-trypsin inhibitor (IαI), a marker of chronic inflammation. Abnormal decorin isoforms and increased expression of transforming growth factor beta-1 (TGF-β1) have also been observed, potentially affecting collagen turnover and tissue remodelling. Increased BMP2 expression has additionally been documented in affected ligaments and skin tissues^5,6,7. 

Recent evidence suggests DSLD is likely a polygenic disorder. Genome-wide association studies have identified pathways associated with extracellular matrix (ECM) homeostasis, proteoglycan metabolism, and hedgehog signalling. Furthermore, an association between DSLD and pituitary pars intermedia dysfunction (PPID) has been reported, raising the possibility that endocrine dysfunction and cortisol dysregulation may contribute to disease development^1,8. 

Relationship with Other Musculoskeletal Disorders 

SL injury frequently occurs alongside other musculoskeletal abnormalities. Experimental studies have demonstrated that partial transection of the medial SL branch increases strain on the lateral condylar surface of the third metacarpal bone (MC3), potentially increasing fracture risk. Clinical studies have similarly linked moderate SL branch lesions with suspensory apparatus failure and metacarpal condylar fractures⁹. 

MRI investigations have revealed cortical bone pathology in many horses diagnosed with SL disease. Complete or partial SL lacerations have been identified in all reported cases of fatal fractures involving the proximal sesamoid bones, third metacarpal bone, or condyles¹⁰. Additionally, approximately 70% of horses with splint bone fractures exhibit concurrent suspensory desmitis. 

Sesamoiditis has emerged as an important risk factor, increasing the likelihood of future SL branch injury by five-fold in yearlings entering training. Subclinical ultrasonographic abnormalities within the SL branch have also been associated with sesamoiditis^1,11. 

Conclusion 

Although suspensory ligament injuries are common and often occur alongside other musculoskeletal disorders, significant gaps remain in understanding the underlying biological mechanisms. Further research is needed to clarify the cellular, genetic, and biomechanical factors contributing to injury development and progression. 

References

1. Guest DJ, Birch HL, Thorpe CT. A review of the equine suspensory ligament: Injury prone yet understudied. Equine Veterinary Journal. 2025 Sep;57(5):1167-82. https://beva.onlinelibrary.wiley.com/doi/pdfdirect/10.1111/evj.14447

2. Dyson S, Pinilla MJ, Bolas N, Murray R. Proximal suspensory desmopathy in hindlimbs: magnetic resonance imaging, gross post‐mortem and histological study. Equine veterinary journal. 2018 Mar;50(2):159-65. https://doi.org/10.1111/evj.12756

3. Bowser JE, Elder SH, Pasquali M, Grady JG, Rashmir‐Raven AM, Wills R, Swiderski CE. Tensile properties in collagen‐rich tissues of Q uarter H orses with hereditary equine regional dermal asthenia (HERDA). Equine veterinary journal. 2014 Mar;46(2):216-22. https://doi.org/10.1111/evj.12110

4. Momen M, Brauer K, Patterson MM, Sample SJ, Binversie EE, Davis BW, Cothran EG, Rosa GJ, Brounts SH, Muir P. Genetic architecture and polygenic risk score prediction of degenerative suspensory ligament desmitis (DSLD) in the Peruvian Horse. Frontiers in genetics. 2023 Aug 14;14:1201628. https://doi.org/10.3389/fgene.2023.1201628

5. Luo W, Sandy J, Trella K, Gorski D, Gao S, Li J, Brounts S, Galante J, Plaas A. Degenerative suspensory ligament desmitis (DSLD) in Peruvian Paso horses is characterized by altered expression of TGFβ signaling components in adipose-derived stromal fibroblasts. PloS one. 2016 Nov 30;11(11):e0167069. https://doi.org/10.1371/journal.pone.0167069

6. Young M, Moshood O, Zhang J, Sarbacher CA, Mueller PE, Halper J. Does BMP2 play a role in the pathogenesis of equine degenerative suspensory ligament desmitis?. BMC Research Notes. 2018 Sep 18;11(1):672. https://doi.org/10.1186/s13104-018-3776-9 

7. Haythorn A, Young M, Stanton J, Zhang J, Mueller PO, Halper J. Differential gene expression in skin RNA of horses affected with degenerative suspensory ligament desmitis. Journal of Orthopaedic Surgery and Research. 2020 Oct 7;15(1):460. https://doi.org/10.1186/s13018-020-01994-y

8. Hofberger SC, Gauff F, Thaller D, Morgan R, Keen JA, Licka TF. Assessment of tissue-specific cortisol activity with regard to degeneration of the suspensory ligaments in horses with pituitary pars intermedia dysfunction. American journal of veterinary research. 2018 Feb 1;79(2):199-210. https://avmajournals.avma.org/view/journals/ajvr/79/2/ajvr.79.2.199.xml

9. Hill AE, Gardner IA, Carpenter TE, Lee CM, Hitchens PL, Stover SM. Prevalence, location and symmetry of noncatastrophic ligamentous suspensory apparatus lesions in C alifornia T horoughbred racehorses, and association of these lesions with catastrophic injuries. Equine veterinary journal. 2016 Jan;48(1):27-32. https://doi.org/10.1111/evj.12367

10. Spargo KE, Rubio-Martinez LM, Carstens A, Wheeler DP, Fletcher L. Catastrophic musculoskeletal injuries in Thoroughbred racehorses on racetracks in Gauteng, South Africa. Journal of the South African Veterinary Association. 2019 Jan 1;90(1):1-5. https://doi.org/10.4102/jsava.v90i0.1640
11. Plevin S, McLellan J, O'Keeffe T. Association between sesamoiditis, subclinical ultrasonographic suspensory ligament branch change and subsequent clinical injury in yearling Thoroughbreds. Equine veterinary journal. 2016 Sep;48(5):543-7. https://doi.org/10.1111/evj.12497