Tendons and Ligaments: Dubai International Equine Symposium

The Dubai International Equine Symposium brought together researchers and practitioners from around the world to discuss soft tissue structures and injuries in the horse (The Horse of May, 1996, page 28). The basic anatomy and physiology of tendons and ligaments is complex. Nathalie Crevier, DVM, of the Clinique Equine-Laboratorie D'Anatomie in France, revealed what has been learned of the microanatomy of tendons and ligaments.

Tendons have a crimped, waveform appearance when seen in longitudinal histologic sections, said Crevier.

"This structural waveform allows the collagen fibers of tendon to be stretched by 3-5% without causing structural damage, since the crimp just unfolds during initial loading," she said. "After this initial elastic phase of tendon elongation comes a stiff, viscoelastic phase during which mechanical damage occurs until rupture at about 8-12% strain."

Studying the angle, length, or how often these crimps or waveforms appear might potentially tell researchers where failure will occur in a tendon or ligament.

"Both the wavelength and the angle of the crimp may vary among fibers within a fascicle, which means that some fibers will straighten out before others as the tendon is stretched," she explained. "Consequently, when a tendon is stretched to failure, a sequence of fibril failures occurs, resulting in a partial rupture, as can be seen in many cases of tendinitis."

In her presentation, Crevier noted that other researchers had described differences found between the superficial digital flexor tendon and the deep digital flexor tendon from the same animal, between different regions in the same tendon, between tendons in horses of different ages, and between the superficial digital flexor tendon in the forelimbs and hindlimbs of the same animal. Earlier research also had shown that superficial and deep digital flexor tendons are very similar in the fetus: "They are composed of many longitudinally arranged cells with plump, granular nuclei between which lie eosinophilic collagen fibers."

Research has shown that metacarpal and metatarsal region tendons from 2-year-old horses look very much like those of neonates, except that their cell nuclei are slightly more elongated, she noted. However, after two years of age, the number of cells decreases and the nuclei lengthen.

In a study Crevier did with 30 horses from one-half hour old to 23 years of age, she confirmed that cellularity (number of cells) was significantly higher in foals than older horses, and that it decreased progressively with age.

"The waveform of collagen fibers also appear significantly more pronounced in foals than in horses of two years or more," she noted. "In two 23-year-old horses of that study, the fibers were almost straight."

Physiology

In contrast to previously held beliefs, Roger K. W. Smith, MA, Vet MB, CerEO, MRCVS, of the Royal Veterinary College in England, has shown that tendon has a "surprisingly good blood supply.

"Tendon is not an avascular structure, and the regulation of blood flow may have important implications in the adaptation and injury of equine flexor tendons," he noted.

Research from Smith and others indicated that there is great variation in blood flow in different tendon structures, and in different areas of the same structure. His research showed that exercise induced an increase in blood flow, although this increase was delayed in unfit animals. There is also the knowledge that some areas of tendon receive nutrition by diffusion from the synovial sheath.

Smith also touched on research involving glycosaminoglycans, or GAG (a side chain of sugars accompanying a protein core that form different proteoglycans in connective tissues; see The Horse of July 1995, page 35). Proteoglycans are vital in the maintenance of the structural integrity of the tissue, either by playing structural roles or by regulating the metabolism of the tissue, noted Smith.

The GAG component of the proteoglycans have been divided into groups: Chondroitin sulphate (CS), the most abundant GAG in connective tissues; dermatan sulphate (DS), constructed similar to CS and present in non-osseous and non-collagenous connective tissues; keratan sulphate (KS), which was thought originally to be restricted to cartilage, cornea, and intervertebral disc, but has been found in a number of other tissues, including tendon (Smith noted that KS is thought to be a "stand-in" for CS in areas with less oxygen); heparin (H) and heparan sulphate (HS), which is involved in inhibiting blood coagulation (H) and in the presentation of growth factors to cells (HS); and hyaluronic acid (HA), which forms aggregates with the large proteoglycan aggrecan to produce a dense, meshwork capable of absorbing water and resisting compression.

Smith noted that tendon is mainly resisting tension, while cartilage is predominately resisting compression, "but both of these forces may stimulate the production of similar, but specific, macromolecules."

A new structural protein identified in human studies that is in increased quantities when there is active tendon and cartilage remodeling going on is cartilage oligomeric matrix protein, or COMP.

"Because of its structure and size, COMP is likely to be a structural protein, and we hypothesize that, based on its distribution and variation with age, it is synthesized in response to loading," noted Smith. "COMP may therefore be a measure of tendon remodeling and/or degree of training, and may provide valuable information on the reaction of tendon tissue to exercise and injury. Studies are currently in progress to assess its usefulness as a serum marker of tendon disease."

Degenerative Disease In Tendons

Roy Pool, DVM, PhD, Emeritus Professor of Pathology at the University of California, Davis, was the musculoskeletal pathologist for the Pathology Service in the Veterinary Medical Teaching Hospital for 25 years. During that time, he dissected and made histopathologic examinations of a large number of normal and diseased digital flexor tendons and suspensory ligaments of horses while performing hundreds of equine necropsies.

He said it was his opinion that: "Many or most acute clinical episodes of catastrophic tendinitis (bowed tendon) occur at sites of accumulative microinjury in tendon tissue." He went on to say that these areas had structural damage that had not been sufficient to provoke internal bleeding and initiate a repair response.

"At least some of the episodes of acute tendinitis of the superficial digital flexor tendon occurred in tendons that contained previous sites of tendon injury and ineffective repair," he noted. "Tendons of these horses probably produced sufficient clinical signs for the horse to be rested, but horses having milder tendon injury may have gone unrecognized."

In a study to observe the effect on corticosteroid injections in tendons, Pool noted that it was apparent that insertion of needles directly into a solid collagenous attachment such as a tendon or ligament was likely to produce laceration and disruption of collagen bundles, "a practice that would defeat the purpose of administrating a therapeutic anti-inflammatory medication."

There is still much to be learned about soft tissues and how to properly maintain or repair them in the athletic horse, but giant strides are being made in understanding the structures, and how they can be treated.

About the Author

Kimberly S. Brown

Kimberly S. Brown was the Publisher/Editor of The Horse: Your Guide To Equine Health Care from June 2008 to March 2010, and she served in various positions at Blood-Horse Publications since 1980.

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