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Degenerative Suspensory Ligament Desmitis (DSLD) is a progressive and often debilitating condition in horses, traditionally believed to be limited to the suspensory ligaments of the limbs. It primarily affects Peruvian Pasos, Arabians, Thoroughbreds, American Saddlebreds, Quarter Horses, and some European breeds. Horses with DSLD often experience chronic pain, progressive lameness, and may ultimately require euthanasia due to quality-of-life concerns.
Emerging research reveals that DSLD is not confined to ligaments—it is in fact a systemic connective tissue disorder driven by abnormal accumulation of proteoglycans.
Proteoglycans are essential molecules found in connective tissues. They provide structural integrity and regulate cell signalling, hydration, and elasticity. However, excessive or misplaced proteoglycan accumulation can disrupt tissue architecture and function.
A study examining 28 DSLD-affected horses (including 22 Peruvian Pasos) and 8 healthy controls uncovered:
Due to the systemic nature of the disorder and the central involvement of proteoglycans, researchers propose renaming DSLD to:
This new name reflects:
Currently, there are no reliable diagnostic tests for asymptomatic horses. Diagnosis is typically based on:
Management Is Supportive Only:
Unfortunately, no treatment currently halts the proteoglycan accumulation at the root of ESPA. Genetic predisposition appears likely, making breeding selection and early detection areas of future focus.
Proteoglycans are no longer a side note—they are the central player in DSLD. The condition once thought to be limited to ligament wear and tear is now recognised as a complex, systemic disease of connective tissue metabolism.
It opens new research avenues for diagnosis, treatment, and genetic studies It shifts how veterinarians and horse owners identify and manage at-risk animals It justifies the adoption of the term ESPA to better reflect the true nature of the disease
Excess glucose is not stored as glucose or glycogen in the connective tissues of horses with DSLD. Instead, glucose may indirectly contribute to DSLD pathology by serving as a precursor for glycosaminoglycan synthesis, potentially amplifying the excessive proteoglycan accumulation characteristic of the disease. High-sugar or high-starch diets could exacerbate this process by increasing glucose availability and causing metabolic stress (e.g., insulin resistance, systemic inflammation), but there is no direct evidence that glucose accumulates in connective tissues. The primary driver of DSLD remains genetic, with proteoglycan dysregulation linked to molecular factors like BMP2. Managing dietary NSC intake (keeping it at 10-12% of the diet) may help reduce metabolic stress in DSLD-affected horses, but it does not address the underlying genetic pathology.
