Short CommunicationSystemic Proteoglycan Deposition Is Not a Characteristic of Equine Degenerative Suspensory Ligament Desmitis (DSLD)
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.
Section snippets
Materials and Methods
Six Peruvian Paso (P1–P6) horses, diagnosed as having DSLD by clinical examination and ultrasonography following the criteria of Mero and Scarlett,4 were compared with two unaffected Quarter horses and an unaffected Standardbred. After euthanasia, a necropsy was performed. Tissue sampling included the suspensory ligament (body and both branches) and the superficial (SDF) and deep (DDF) digital flexor tendons of all four limbs as well as the quadriceps muscle, diaphragm, nuchal ligament, tongue,
Results
A synopsis of histologic and histochemical results is summarized in Table 1 (affected horses) and Table 2 (control horses). In all six of the affected horses, the suspensory ligaments and superficial and flexor tendons displayed typical DSLD lesions.2 In two horses the lesions were scored as “marked”; and in four, “severe.” By contrast, in the control horses (Table 2), most of the specimens were negative for histologic lesions or for PG staining. However, each had occasional microfoci of
Discussion
The histopathologic findings in the suspensory ligament and its branches and in the SDF and DDF tendons were similar to those described in lesions of DSLD,2 and also to those described in degenerative tendons and ligaments of athletic horses.11
There were no discernible differences in the histologic appearance of tissues from affected and unaffected horses other than changes present in the suspensory ligaments and flexor tendons of the distal limbs. Many of the specimens from nonaffected horses
Conclusions
DSLD is a complex entity that incorporates genetic as well as molecular, conformational, and functional elements in its pathogenesis. A systemic mechanism affecting tissues other than tendons and ligaments of the limbs may well be at play, but we have found no convincing evidence that the syndrome is a consequence of, or results in, a systemic proteoglycan accumulation.
References (19)
- et al.
Diagnostic criteria for degenerative suspensory ligament desmitis in Peruvian Paso horses
J Equine Vet Sci
(2005) - et al.
The localization of proteoglycan by light and electron microscopy using safranin O: a study of epiphyseal cartilage
Ultrastruct Mol Struct Res
(1976) Degenerative suspensory ligament desmitis
Hoofcare and Lameness
(1993)- et al.
Twenty cases of degenerative suspensory ligament desmitis in Peruvian Paso horses
AAEP Proc
(2002) - et al.
Degenerative suspensory ligament desmitis as a systemic disorder characterized by proteoglycan accumulation
Biomed Central Vet Res
(2006) Chemical basis of the histological use of safranin-O in the study of articular cartilage
J Bone Joint Surg
(1971)- et al.
Simultaneous localization of proteoglycan by light and electron microscopy using toluidine blue O: a study of epiphyseal cartilage
J Histochem Cytochem
(1976) - et al.
Picrosirius staining plus polarization microscopy, a specific method for collagen detection in tissue sections
Histochem J
(1979) - et al.
Alteration and recovery of the spatial orientation of the collagen network of articular cartilage in adolescent rabbits following intra-articular chymopapain injection
Connect Tissue Res
(1996)
Cited by (19)
Ultrasonographic Evaluation of the Suspensory Ligament in Quarter Horses Used for Cutting
2022, Journal of Equine Veterinary ScienceCitation Excerpt :Lameness associated with the suspensory ligament (SL) and the surrounding tissues, known as proximal suspensory disease (PSD), has been well documented in several types of horses [1–11]. Pathologies can involve the proximal suspensory ligament (PSL), the SL body, SL branches, the enthesis of the SL origin at the palmar/plantar cortex of the third metacarpal and metatarsal bones (MCIII, MTIII), and/or surrounding fascia and nerves [6–9,12–22]. It is currently accepted that PSD is a multifactorial disease and several factors may predispose horses to this condition.
Regenerative Therapies for the Treatment of Tenodesmic Injuries in Horses
2019, Journal of Equine Veterinary ScienceCitation Excerpt :The association between DSLD and pituitary pars intermedia dysfunction (PPID) has been suggested because of incidental findings of a reduced arrangement of collagen and proteoglycan accumulations in SL of horses with PPID [94]. However, this situation remains controversial because of the high concentrations of proteoglycans present in the aorta and the nuchal ligament having been found in healthy horses compared with horses with DSLD [95]. Recently, findings of endochondral ossification have been described for SL injury without proteoglycan accumulation [67], contradicting the hypothesis of a systemic proteoglycan abnormality.
Effects of athletic conditioning on horses with degenerative suspensory ligament desmitis: A preliminary report
2011, Veterinary JournalCitation Excerpt :At the microstructural level, there is degeneration and swelling of collagen bundles (Mero and Pool, 2002). Excessive proteoglycan deposition has also been identified in the suspensory apparatus of horses with DSLD (Mero and Pool, 2002; Mero and Scarlett, 2005; Halper et al., 2006; Schenkman et al., 2009). Defective ligament healing by abnormal fibroblasts results in fibrocartilage instead of collagen deposition following microdamage (Mero and Pool, 2002; Halper et al., 2006).
Connective Tissue Disorders in Domestic Animals
2021, Advances in Experimental Medicine and Biology