Systemic Proteoglycan Deposition Is Not a Characteristic of Equine Degenerative Suspensory Ligament Desmitis (DSLD)

Abstract

Recently Degenerative Suspensory Ligament Desmitis (DSLD) has been proposed to be a disease characterized by systemic deposition of proteoglycan (PG) in connective tissues. To investigate this hypothesis, 6 clinically affected Peruvian Paso horses were compared to 2 unaffected quarterhorses and one unaffected standardbred. Histological sections of limb ligaments and tendons, nuchal ligaments, aortas, hearts, eyes, visceral organs and brains from both groups were stained with H&E as well as special stains for PG. Safranin-O stained sections were found to be optimal for elucidating the presence of PG. Although lesions characteristic of DSLD were present in suspensory ligaments of each clinically affected horse, including foci of chondroid metaplasia with abundant PG, a similar but less pronounced pattern of PG deposition was present in control horses. In contrast to findings of the previous study, PG deposition was not unique to DSLD horses, and PG deposition in aortas and nuchal ligaments of some control horses exceeded levels of PG present in similar tissue of DSLD horses. Furthermore, the “vascular lesion” described in the media of arteries as cellular separation and intercellular amorphous matrix deposition was within the spectrum of changes recognized in both affected and unaffected horses. We found no evidence that DSLD is a systemic PG deposition disease.

Introduction

Degenerative suspensory ligament desmitis (DSLD) is a progressive disorder primarily affecting the suspensory ligaments in horses of several breeds.¹ It results in progressive deterioration of the suspensory ligaments and flexor tendons leading to severe lameness and pain. Limb involvement is frequently bilateral or quadrilateral.

Gross appearance of transverse sections of chronic DSLD lesions is characterized by increased diameter of the body and branches of the suspensory ligament. Histopathologic changes have been described in the suspensory ligament and its branches and in the flexor tendons.² Prominent findings in the early lesions in suspensory ligaments include clusters of fibroblasts and fibrocartilage metaplasia. Affected fascicles are swollen and pale, and their collagen fibers are acellular and fibrillated, resulting in the merging of fibrillated collagen bundles of adjacent fascicles to form megafascicles. Granulation tissue arising in interfascicular septa makes abortive attempts at fascicular repair.

The consequence is a characteristic clinical picture with severe functional impairment and a distinctive ultrasonographic appearance.² DSLD has a familial distribution, although a definite pattern of inheritance has not been established. The pathogenesis has not been determined, and there is no successful treatment.

A recent publication postulated that DSLD is a systemic disorder involving the deposition of proteoglycan (PG).³ This study was designed to answer a specific question: Are the histopathologic changes that characterize lesions of DSLD limited to the lower extremities of affected horses, or is there evidence of an abnormal systemic proteoglycan distribution elsewhere in the connective tissues of affected horses?

To that effect, we reviewed the histopathologic and histochemical changes in the suspensory ligaments and flexor tendons in all four extremities and other connective tissues and organs of six horses affected with DSLD and three unaffected control horses.