Platelets Might Play Early Role in Laminitis

Laminitis begins well before clinical signs occur, at the cellular or even the molecular level, and addressing platelets might be a key to prevention or early treatment. Jamie Textor, DVM, Dipl. ACVS, an equine surgeon and PhD candidate at the University of California, Davis, spoke about the role of platelets in laminitis during the Sept. 17-18 Laminitis West Conference, in Monterey, Calif.

Inflammation is central to most cases of laminitis, and Textor discussed cellular events that happen before that inflammation manifests itself in clinical signs.

"Early on, we're talking about cellular events," Textor said. "That's going to be the best opportunity we have to intervene, by understanding the cellular processes and trying to target some of them before they become a vicious cycle."

The components of laminitic inflammation at the cellular level are neutrophils, platelets, and monocytes. Textor focused on platelets because research indicates that they are inflammatory cells, are very sensitive to endotoxins, and might be the first responders in laminitis.

When platelets activate, they aggregate or clot (creating blood clots to stem bleeding) and then change shape radically. They also contain and release vasoconstrictors, and that restriction of blood flow in the foot could lead to laminitis. Textor cited a 1998 study showing that inhibiting platelet activation prevented laminitis in experimental setups. Subsequent studies have confirmed that platelet aggregation is an early indicator of laminitis.

"We've got a triple threat here," said Textor. "We've got our platelets activating early, probably the very first response. We've got the neutrophils (a type of white blood cell) getting activated. They start interacting with the endothelium (lining of blood vessels) and start to go across it (into the laminae). After that time, laminar breakdown begins."

Knowing this sequence of events might allow veterinarians to develop potential therapeutic strategies. Speaking generally about approaches to prevention, Textor said, "We could prevent these cells from ever getting (to the laminae) or ever being activated. We could block the things that they deliver--we could prevent the vasoconstrictors from doing their thing. Lastly, maybe we could enhance the protective mechanisms that tissue might already have in place."

About the Author

Tracy Gantz

Tracy Gantz is a freelance writer based in Southern California. She is the Southern California correspondent for The Blood-Horse and a regular contributor to Paint Horse Journal, Paint Racing News, and Appaloosa Journal.

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